A couple of readers asked me to look into research on the use of frequencies in cancer and what has been studied or approved to date.

So I started digging.

But first, I’d like to share my own experience with bioresonance.

Someone recommended a practitioner who used a machine that worked with energetic fields. Since I am open to many different options, I decided to visit him with a friend and booked a session.

Here’s what happened.

He placed two electrodes on my head and connected them to a machine. As the program ran, the screen displayed a list of health issues, the percentage of “off” frequencies for each and what needed to be balanced. According to the practitioner, the machine could scan for more than 2,000 conditions across biological and psychological systems.

It moved through the body area by area and highlighted where it found problems.

Some of the main findings struck me:

• It showed breast cancer—correct, although I was already in remission.

• It showed an increased risk of gastroesophageal cancer, which matched a risk identified through separate testing.

• It showed many smaller issues. Some I knew about and others I did not.

After around 20 minutes, the practitioner reviewed the results. He then said the machine could reset the frequencies to where they needed to be.

He pressed a button and the screen moved through each finding again. One by one, the frequencies appeared as corrected. This part took another 20 to 30 minutes.

I left with two very different impressions. The scan had identified several things that appeared surprisingly accurate. For someone as skeptical as me, it was quite impressive.

However, I also realized I had no way to know whether the “correction” on the screen had produced a biological change in my body.

That distinction is central in how I interpret the research I found.

So, What Exactly Is Bioresonance?

Bioresonance is not one single technology.

The machine I experienced belonged to the scan-and-correct side of the field. These systems may use a headset, hand sensors or electrodes. Software compares the reading with a database of organs, tissues, microbes and health conditions. The results may appear as percentages, colors or levels of energetic stress. The same system may then send selected frequencies back.

Other practitioner systems work through electrodes placed on the hands, feet or other parts of the body. They aim to collect very low electrical or electromagnetic signals from the patient.

The theory proposes that cells, organs, allergens, toxins and microbes have their own frequency patterns. Illness or stress can disrupt the body’s normal electromagnetic communication.

The body produces measurable electrical activity, so the wider idea that biological processes can respond to electrical signals is plausible. Whether each disease produces a unique frequency pattern that these machines can reliably detect is the larger question.

The device filters the signal into different frequency ranges. Some systems aim to separate “harmonious” patterns from “disharmonious” ones. The selected signal may then be amplified, weakened or inverted before it is returned through another electrode.

Inversion is often compared with noise-canceling headphones. They produce an opposing sound wave to reduce unwanted noise. Bioresonance aims to do something similar with a disruptive pattern in the body.

Some practitioners also place sealed samples of foods, allergens, supplements or other substances in a connected testing unit. The machine then looks for a response between the patient and the frequency pattern associated with that substance.

Testing and treatment can happen during the same session. The machine first identifies a possible stress or imbalance and then selects a program intended to correct it.

What Have Bioresonance Studies Found?

There is some research behind bioresonance. Most clinical studies are small, although several produced interesting results.

Functional Digestive Symptoms

A randomized placebo-controlled trial studied 20 people with functional gastrointestinal complaints. Ten received active bioresonance and ten received sham treatment.

The active group reported significant reductions in the frequency and intensity of digestive symptoms. Stomach pain and bloating also improved. Intestinal sounds did not change significantly.

The sample was tiny. Yet the use of sham treatment makes the result more useful than a series of patient reports.

Smoking Cessation

A larger double-blind study tested a bioresonance method in 190 smokers. Half received active treatment and half received a sham version.

After one week, 77.2% of the active group reported that they had stopped smoking compared with 54.8% of the control group. At one month, the figures were 51.1% and 28.6%.

After one year, 28.6% of the active group and 16.1% of the sham group reported that they remained smoke-free. Participants in the active group also reported less desire to smoke.

That was a strong result for a double-blind pilot study. Smoking status came from telephone interviews rather than nicotine or carbon monoxide testing. Independent replication with biochemical confirmation would make the finding much stronger.

Knee Osteoarthritis

A study in 75 people with knee osteoarthritis compared standard treatment with standard treatment plus bioresonance.

The overall response rate was 94% in the bioresonance group compared with 57.5% in the standard-treatment group. Signs of synovitis and tendinitis also improved in 75% of the combined group compared with 32.5% of those receiving standard treatment alone.

The difference extended beyond short-term pain relief. Benefits in the bioresonance group lasted for up to 12 months while pain began to worsen again by six months in the standard-treatment group.

This points toward an added and possibly longer-lasting effect from bioresonance. The study was not sham-controlled, so expectations may have influenced pain reporting. The changes in joint inflammation make the findings more interesting than a purely subjective improvement.

Lymphedema And Lipedema

A pilot study combined bioresonance microcurrents with the transdermal delivery of active substances in people with lymphedema or lipedema.

Limb volume fell by around 2% after six days. Patients also reported less heaviness, pain and altered sensation.

There was no separate control group and two treatments were used at once. That makes it impossible to know how much of the result came from the microcurrents, the transdermal substances or the combination.

These studies point to possible effects in several conditions. Other research found no benefit.

When The Signal Went Quiet

A double-blind study followed 32 children with long-standing atopic dermatitis. All received conventional inpatient care plus either active or sham bioresonance.

Both groups improved. Active bioresonance did not add a measurable benefit.

A small study in 14 children with stuttering also found no clear improvement from bioresonance.

These studies used different systems and programs for different conditions. They are not one test of the entire field. They show that bioresonance can be studied with sham controls and that the results so far are mixed.

The populations, conditions, treatment schedules and ways of measuring success also differed.

So can any of this apply to cancer?

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Does Cancer Have Its Own Frequency Signature?

Researchers began exploring this question by testing frequencies in people with cancer.

A handheld generator emitted low-level radiofrequency electromagnetic fields while researchers changed the modulation frequency. They monitored patients for changes in pulse amplitude.

Certain frequencies repeatedly produced a response. Patients with the same cancer often reacted to many of the same frequencies. Researchers eventually identified groups associated with breast, liver, prostate and several other cancers.

They then took those frequency sets into the laboratory.

Liver and breast cancer cells were exposed to cancer-specific or randomly selected modulation frequencies. The liver frequencies reduced growth in liver cancer cells. The breast frequencies did the same in breast cancer cells.

The random frequencies did not produce the same effect. The response depended on the match between the frequency set and the cancer type.

This was an important finding. The cells did not simply respond to any electromagnetic exposure. The biological effect was frequency-specific.

What Happened Inside The Cancer Cells?

Further research found that the liver cancer frequencies activated a calcium channel called Caᵥ3.2.

This raised calcium inside the cancer cells and pushed them toward differentiation. Differentiated cells take on more normal features and lose some of their ability to multiply.

The treatment also reduced cancer stem cell markers and tumor-sphere formation. Both have been linked to treatment resistance, recurrence and metastasis.

This gave researchers a possible biological mechanism. The frequencies were not simply “balancing energy.” They appeared to interact with a specific channel on the cancer cells and change signals inside them.

From Frequency Lists To Patients

The same approach then moved into patients.

A phase I/II study included 41 people with advanced liver cancer who had few remaining treatment options. Patients placed a spoon-shaped antenna in the mouth for one hour three times a day.

A 27.12 MHz carrier wave delivered 194 modulation frequencies associated with liver cancer. The carrier wave acted as the vehicle for the lower modulation frequencies. The signal was too weak to heat the tissue.

Fourteen patients, or 34.1%, had stable disease for more than six months. Three had partial responses and one had a near-complete response. That amounts to an objective response in almost 10% of the group.

Median progression-free survival was 4.4 months and median overall survival was 6.7 months.

For context, a major sorafenib trial in advanced liver cancer reported median survival of 10.7 months with sorafenib and 7.9 months with placebo. Those patients generally had better liver function and received sorafenib as first-line treatment, so the two trials cannot be compared directly. Sorafenib produced partial responses in only 2% of patients and no complete responses.

The 6.7-month survival in the frequency study did not establish a survival benefit. The more interesting finding was the combination of prolonged stable disease, an objective response rate of almost 10% and very low toxicity in people with limited options. Researchers reported no grade 2, 3 or 4 treatment-related toxicities.

These results were promising enough to take the technology further. In 2023, the FDA allowed the device onto the US market through a Humanitarian Device Exemption for adults with advanced hepatocellular carcinoma that had stopped responding to first- and second-line treatments.

This pathway is based on safety and “probable benefit.” It does not require the same level of effectiveness data as full premarket approval.

Access remains limited. In December 2024, Karmanos Cancer Institute in Michigan announced that it had become the first center in the world to prescribe the at-home treatment.

Does This Validate Consumer Bioresonance?

The cancer research supports the wider principle that specific frequencies can affect cancer cells. It does not automatically validate every bioresonance system since their technology and delivery methods vary widely.

My own experience shows why detection and correction need to be separated. Several findings from my scan matched my health history, which made me curious about what the machine could detect.

Yet when the screen changed each result from “off” to “corrected,” no second biological measurement showed that anything in my body had changed.

The published studies give me a reason to remain interested. Some controlled trials produced meaningful results while others found no benefit.

Personal stories can also point toward effects worth studying, although they cannot show what caused a remission when standard treatment, supplements, diet and frequency therapies were used together.

So, can frequencies treat cancer?

The short answer is yes.

Specific frequencies can affect cancer cells and a tumor-specific frequency device is now authorized for a defined group of patients with advanced liver cancer. Their future in cancer care will likely depend on precision: the right frequency, intensity and delivery method for a defined cancer type or biological target.

The question now is whether these findings will translate into effective treatments for more cancers and how far the field can go.

Much of what I share comes from years of researching and making decisions during my own cancer journey. I share this as personal research and perspective for educational purposes only. Please consult your healthcare team before making treatment decisions, including decisions about supplements or medications.

References

Nienhaus J, Galle M. Placebo-controlled study of the effects of a standardized MORA bioresonance therapy on functional gastrointestinal complaints. Forschende Komplementärmedizin. 2006.

Pihtili A et al. Evidence for the efficacy of a bioresonance method in smoking cessation: a pilot study. Forschende Komplementärmedizin. 2014.

Maĭko OI, Gogoleva EF. Outpatient bioresonance treatment of gonarthrosis. Terapevticheskii Arkhiv. 2000.

Application of microcurrents of bioresonance and transdermal delivery of active principles in lymphedema and lipedema of the lower limbs: a pilot study. Giornale Italiano di Dermatologia e Venereologia. 2014.

Schöni MH et al. Efficacy trial of bioresonance in children with atopic dermatitis. International Archives of Allergy and Immunology. 1997.

Wille A. Bioresonance therapy in stuttering children. Forschende Komplementärmedizin. 1999.

Zimmerman JW et al. Cancer cell proliferation is inhibited by specific modulation frequencies. British Journal of Cancer. 2012.

Jimenez H et al. Tumor-specific amplitude-modulated radiofrequency electromagnetic fields induce differentiation of hepatocellular carcinoma via targeting Caᵥ3.2 T-type voltage-gated calcium channels and calcium influx. EBioMedicine. 2019.

Costa FP et al. Treatment of advanced hepatocellular carcinoma with very low levels of amplitude-modulated electromagnetic fields. British Journal of Cancer. 2011.

US Food and Drug Administration. TheraBionic P1—H220001. 2023.

Karmanos Cancer Institute. Physicians begin prescribing new FDA-approved radiofrequency electromagnetic device to treat advanced liver cancer. 2024.

Most people who have dealt with cancer, or come close to someone who has, know the word metastasis. It’s the word that scares most and the one that turns a local problem into a body-wide one.

But before cancer cells can spread, they often need to change the way they behave.

A process that can help them do that is called epithelial-to-mesenchymal transition, or EMT.

Welcome to the fifth letter in our ABCs of Cancer Biology series: EMT.

In simple terms, EMT is a cell trading one identity for another, moving from tightly packed and fixed in place to loose and better able to travel.

Most solid tumors start out from cells that behave like bricks in a wall. They sit close together, stay put and face a defined surface. That’s the epithelial state. When those cells start loosening their connections to the wall, they can acquire features that allow them to move through the surrounding tissue. That’s the shift toward a mesenchymal state.

EMT is the process a cell goes through as it moves from the first kind of behavior toward the second. It’s not necessarily a new mutation and the cell’s DNA sequence doesn’t have to change. What changes is which instructions inside that DNA get used.

Importantly, this can happen while the cancer cell is still in the original tumor. EMT can help cells loosen their connections, invade the surrounding tissue and enter blood or lymph vessels. Once tumor cells enter the bloodstream, they become circulating tumor cells, or CTCs.

But EMT isn’t required for every cancer cell to spread. Nor does a cell have to complete the entire transition. Cancer cells can retain epithelial features and travel in clusters. Many occupy a state somewhere between epithelial and mesenchymal. We’ll come back to why that matters below.

Cancer cells are not reinventing the wheel here, though. A developing embryo uses this process to build tissues and organs. Wound healing also uses related EMT programs. Cancer just borrows this tool for its own purposes. That’s also why it’s so hard to shut it off without disrupting other body processes.

The Switches That Flip

A small group of proteins help control EMT. The best known include SNAIL, SLUG, TWIST, ZEB1 and ZEB2 (yes, seriously, the researchers must’ve had some fun here).

They can be activated by signals such as inflammation, low oxygen and growth factors in the tissue surrounding a tumor.

An important consequence is suppression of E-cadherin, a protein that helps epithelial cells stick to each other. You might have seen E-cadherin mentioned on a pathology report, sometimes as “loss of E-cadherin.”

When E-cadherin falls, cells can loosen their connections with neighboring cells and start expressing proteins associated with movement and invasion.

Loss of E-cadherin alone doesn’t prove that EMT is happening, however. It’s one feature associated with the process and can occur for other reasons.

Another epithelial marker that can fall during EMT is EpCAM. This one matters practically, not just biologically.

Many CTC tests have traditionally relied on EpCAM to capture circulating tumor cells. If a cancer cell shifts far enough away from an epithelial state, EpCAM can fall enough that an EpCAM-dependent test may miss it.

The cell hasn’t necessarily disappeared. It may simply have changed enough that the tool designed to detect it no longer recognizes it. That’s why CTC numbers need to be interpreted in the context of the technology used in a liquid biopsy and what kind of cells it actually measures.

The Dangerous Middle

For a long time, EMT was described as a simple switch: a cell was either epithelial or mesenchymal.

The reality is much messier.

Many cancer cells sit somewhere in between. They keep some epithelial traits while acquiring mesenchymal ones. Researchers call these hybrid epithelial/mesenchymal states, or partial EMT.

In many experimental models, these hybrid states appear to be particularly dangerous.

They can retain enough cell-to-cell adhesion to travel together in clusters while gaining the mobility needed to invade. CTC clusters can be particularly efficient at establishing metastases compared with individual circulating tumor cells.

EMT also isn’t necessarily a one-way trip.

A cell can shift toward the mesenchymal side and later move back toward an epithelial state. That reverse process is called mesenchymal-to-epithelial transition, or MET. It may help disseminated cells settle and grow at a new location.

This ability to move between states is called plasticity.

Treatment can also create selection pressure: cells that are vulnerable die while those better able to adapt and survive remain.

Together, plasticity and selection help explain how a tumor can change under pressure rather than remaining one fixed target. That also explains why it can be so difficult to target tumors with a single drug.

The Link To Cancer Stem Cells

If you read the C as in CSCs article in this series, this next part will feel familiar.

The same proteins involved in EMT can also push cancer cells toward stem-like states associated with treatment resistance and the ability to rebuild a tumor.

A landmark 2008 study showed that inducing EMT in experimental breast epithelial cells generated cells with stem-cell-like properties, including increased self-renewal and tumor-initiating ability.

Not every cell undergoing EMT automatically becomes a cancer stem cell. But EMT and stemness are closely connected biological programs.

That’s why a shift toward more mesenchymal features can sometimes appear together with increasing stem-like features.

I’ve seen something like this in my own liquid biopsy testing from two different companies. There was a partial loss of EpCAM while stem-like features increased.

It’s not good news to observe, but here it is. Biology at work.

It’s not a guarantee of metastasis. These tests can’t tell whether an individual circulating cell will ever successfully seed one. But after a year and a half of mostly stable liquid biopsy results, it’s nevertheless not a change I like to see.

More Than A Ticket Out

EMT isn’t only about movement.

Cells activating parts of this program can also become harder to kill. EMT has been associated with resistance to chemotherapy and radiation through several mechanisms. Cells can avoid apoptosis, alter their response to damage and enter slower-growing states known as quiescence.

They can also affect the immune system.

Cells activating EMT programs can carry more PD-L1 on their surface, a protein that helps suppress an immune attack. EMT-related signaling and PD-L1 can also reinforce each other in cancer models.

So the same biological shift can potentially help a cancer cell move, survive treatment and evade parts of the immune response.

Remember the E-cadherin loss I mentioned above?

No one ever explained to me what it meant when it appeared on my original pathology report. I now understand that the E-cadherin loss present at diagnosis was a feature associated with EMT. It doesn’t prove my tumor was undergoing EMT, but today I look differently at what that finding meant.

Can EMT Be Influenced?

In the next section, we’ll look at what the research says about targeting this process, including several natural compounds and repurposed drugs that have shown effects on EMT pathways, cancer cell plasticity and the shift back toward a more epithelial state. We’ll also look at what this evidence can and cannot tell us about their use in people.

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When you’re trying to optimize your health, whether it’s during cancer treatment or thereafter, it’s easy to pile up supplement after supplement with the hope they will all help restore some of the body’s deficiencies.

While I’m a firm believer in the power of vitamins and nutraceuticals, as I’ve seen them support my own body, there is a way of taking those to maximize their effect and delivery in the body.

A supplement can work for you in the morning but not at night. Or vice versa. What matters is the biological environment. And that can change depending on the time of day.

Your body runs in cycles. That’s why you wake up to daylight and sleep at night. This may sound obvious, but I think we tend to forget that the body is made up of billions of cells that make it function. And those cells also have their own circadian rhythms.

Cell Repair vs Cell Growth

As your body rests at night, many cellular processes shift toward maintenance and repair. Cell division, DNA repair, metabolism and immune activity all follow circadian rhythms, although their exact timing differs between tissues and pathways.

Growth hormone, which drives tissue repair and regeneration, is released in pulses during deep sleep, most heavily in the first half of the night.

The immune system doesn’t rest during this window. Instead, it shifts its focus. Certain white blood cells move out of the bloodstream and into lymphoid tissues overnight, where immune surveillance and coordination continue.

At daylight, the priorities shift. Metabolism, activity and feeding become more prominent, while tissues throughout the body continue following their own circadian patterns.

This is not an arbitrary process. It’s the same logic that governs when you feel hungry, when you feel alert and when you feel tired. It just happens to play out at the cellular level instead of the level you can consciously feel.

This is where supplements enter the picture. If the pathways a compound affects fluctuate throughout the day, it makes sense that the biological environment it encounters can change depending on when you take it.

Where Melatonin Fits

Melatonin is the clearest example of this principle, because its entire function is to signal nighttime to the rest of the body.

It acts on the clock itself. It binds directly to receptors in the brain region that sets the master rhythm for every other cell.

Taken in the evening, close to your natural bedtime, it supports the drop in body temperature and alertness that leads into sleep.

Taken at the wrong time, melatonin can shift the circadian clock in the wrong direction and cause sleepiness when you’re trying to be alert.

This is one of the few supplements where the timing research is quite clear.

I would go one step further. Taking melatonin at the same time every evening helps reinforce a consistent signal to the circadian clock. This can help keep your daily rhythm more stable, not just nighttime sleep.

Vitamin D’s Slower Cycle

Vitamin D moves on a longer cycle and interacts with the circadian system in several ways.

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Vitamin E is an antioxidant. And according to what you see on social media, antioxidants are supposed to be good for you. They fight free radicals that damage cells and are often grouped together with vitamin C and other antioxidants for their health benefits.

That reputation pushed researchers to test vitamin E in several cancer settings.

What they found was not what they expected.

In one large trial, men without prostate cancer took vitamin E to try to prevent it. Instead, the men receiving vitamin E developed significantly more prostate cancer than those receiving placebo.

In patients with head and neck cancer undergoing radiation, another trial found a substantially higher rate of second primary cancers during antioxidant supplementation.

Antioxidants were doing exactly the opposite of what researchers assumed they would do.

However, there’s an important nuance cancer patients need to know about. Vitamin E is not one molecule.

It is a family of eight related compounds: four tocopherols and four tocotrienols. They don’t all behave the same way.

Some forms have raised concerns in cancer, while others show very different effects.

Let’s dig in.

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There is a shift cancer patients often feel once other people find out they have cancer. It happens with friends, family and acquaintances. I noticed it in the way they looked at me. I noticed it in the way they worried about me. But more than anything, I noticed it in the unsaid, silent assumptions people carry.

When cancer hits, the patient gets overwhelmed. There is the news itself. There is the immediate question of whether you are going to die. Then there are the appointments, scans and new information that a cancer patient needs to absorb. All of that is real and it can tax the emotional system enormously.

But there is another piece that slips in as the patient is navigating the news. It’s the unsaid part. It becomes something you have to deal with emotionally, mentally and spiritually, on top of the strength already required to manage the biological and medical side of the disease.

It’s the cancer stigma. And it might be one of the heaviest, and most insidious, weights a cancer patient has to carry.

Borrowed Grief

Someone I knew had lost his wife to cancer. Her disease did not respond well to treatment. It kept spreading. She went through surgery after surgery, round after round of chemo, procedure after procedure. Her body couldn’t take it any longer. She passed after several years of trying.

After her death, that man became bitter. He was extremely disillusioned with the medical system and carried deep anger that was still present beneath the surface 12 years later. I am not judging this man. What he and his wife went through was hard. Very hard.

But when I told him my diagnosis, I could feel his experience weighing on my situation before I had even finished the sentence. With every conversation, I felt as though he had pretty much written me off. His past had made him fatalistic and that outlook was now being projected onto me.

In his mind, I had already been placed in the same story as his wife. I could tell he couldn’t even fathom that I might reach a state of NED or remission.

But my cancer was a different type. It had different treatment options. From what I had researched and understood, my prognosis seemed better than hers.

While I was trying to hope, pray and visualize a future with no evidence of disease, his projection kept pulling in the opposite direction. It was like swimming upstream. He was fatalistic. I was not.

When People Mean Well And Still Get It Wrong

Some people carry heavy assumptions about cancer, sometimes rooted in real experience and sometimes not.

One woman I met shortly after my diagnosis had no direct experience with cancer. She was supportive in almost every way she knew how to be. But when hospitals or cancer patients came up, her instinct was to say that hospitals carry negative energy and that cancer patients carry negative energy too.

At the time, I spent many hours inside a hospital-affiliated nonprofit surrounded by fellow patients. The cancer patients I met there were some of the most positive, supportive and loving people I had ever encountered. If anything, it felt like a community built on genuine generosity, humor and compassion.

Stepping Through An Invisible Door

Once people know, you can feel singled out. Like you have stepped through an invisible door that puts you in a separate category. People still see you. They just don’t always look at you the same way.

And this is not just something I felt. Research on cancer-related stigma suggests that many patients experience some version of it.

A German study of 858 patients with breast, colon, lung and prostate cancer found that these experiences were associated with poorer quality of life. Among breast cancer patients, the association extended across physical, psychological, social, spiritual and overall quality of life.

There is also research into something called social constraint: when the reactions of other people make patients feel they need to hold back, alter or avoid expressing what they are thinking and feeling about their cancer.

A meta-analysis of 30 studies found that patients who felt more constrained by other people's reactions also tended to experience higher levels of both general psychological distress and cancer-specific distress.

In other words, the social environment around the patient matters.

Most people who project fear onto a patient are not trying to hurt them. But when someone projects the end of your story before they understand your diagnosis, treatment options or odds, you are not only spending energy dealing with the disease. You are also spending energy managing the people around you.

Fear can also turn into pressure: another treatment, another opinion, another thing the patient “should” be doing. Often that comes from love. But love and fear can coexist, and the patient can end up carrying both.

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Pity Is Not Support

There is one reaction I will not accept from anyone, doctors included: pity.

I remember a doctor who looked at me with pity during an appointment. Not warmth. Not concern. Pity. I cringed inside and I still remember it.

She didn’t mean it in a bad way. But pity was not what I needed.

Pity can make a person feel diminished. Compassion stands beside them. The difference may seem subtle to the person offering it and unmistakable to the person receiving it.

Cancer is an enormous spectrum of diseases, stages, prognoses and treatment possibilities. The word itself tells you little about what will happen to the person sitting in front of you.

Cancer patients do not become phantoms the second that word gets spoken. They’re still normal people.

What Patients Are Actually Asking For

I write this to ask anyone who knows or cares for a cancer patient to pay attention to what their own thoughts and projections might be doing to that patient.

The patient is already spending energy on scans, treatments and decisions. Whatever fear another person brings into the room belongs to that person. While dealing with cancer, a patient should not also have to reassure everyone around them.

I often say everyone is half a step away from being a cancer patient. I do not mean that in a dark way. Cancer is not something that only happens to other people. It can enter any family, at any time.

A few things that help in practice:

• Ask what the patient needs instead of assuming you already know. Do not assume.

• Let the patient set the tone of the conversations, including how much or how little they want to discuss the disease.

• Bring hope, not predictions. If you need somewhere to put your own fear, talk to a friend, a therapist or someone else who can support you.

• Respect the patient’s autonomy. Only offer opinions about treatments or alternatives when they are wanted. Do not turn your own fear into pressure. Ultimately, the decision belongs to the patient.

I know this is not simple for caregivers, friends or family. Fear is a normal response to a frightening diagnosis and no one should be ashamed of feeling it. The burden on caregivers is a whole other subject and should not be underestimated.

But this article is about the needs of the patient.

I still think about the widower who could not separate my diagnosis from his wife’s and about the woman who believed cancer patients carried negative energy. Neither one meant harm. Both brought their own history and beliefs into the room with me.

Recognizing the difference between theirs and mine helped me protect my own hope.

I just wish I didn’t also need to fight that uphill battle on the emotional level while dealing with everything cancer was already asking of me.

Much of what I share comes from years of researching and making decisions during my own cancer journey. I share this as personal research and perspective for educational purposes only. Please consult your healthcare team before making treatment decisions, including decisions about supplements or medications.

References

Ernst J, Mehnert A, Dietz A, et al. Perceived stigmatization and its impact on quality of life: results from a large register-based study including breast, colon, prostate and lung cancer patients. BMC Cancer. 2017;17:741.

Adams RN, Winger JG, Mosher CE. A meta-analysis of the relationship between social constraints and distress in cancer patients. Journal of Behavioral Medicine. 2015;38(2):294–305.

You probably heard some version of this before:

“We all have cancer cells, don’t we?”

“The body clears cancer cells every day.”

"Cancer cells form all the time. Your immune system just gets rid of them."

As a cancer patient, I find these phrases a bit unsettling. They seem to minimize what people with cancer go through, even if that’s not the intention. It can almost make cancer sound like a routine occurrence. And indirectly, as if the patient somehow did something wrong for having those cancer cells eventually show up on a scan.

So let’s take a closer look at what these phrases actually mean.

Does a healthy body really carry cells that count as cancer?

And does a cancer patient carry those same cells every day too?

The short answer is no. These statements contain a kernel of biological truth, but they oversimplify what is actually happening. They also blur the distinction between a healthy cell that has picked up DNA damage and a cell that has already become cancer.

And that’s how we get to D for DNA Repair, the fourth article in the ABC’s of Cancer Biology series.

If you haven’t subscribed yet, I’d be grateful if you considered becoming a free or, even better, a paying subscriber. It allows me to keep researching and writing these in-depth articles about cancer and sharing what I’ve learned along the way.

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Every Cell Is A Work In Progress

Every cell in your body carries a full copy of your DNA. Every time a cell divides, it first has to copy that DNA. Copying billions of letters, over and over, all day every day.

You spend time in the sun? UV light damages DNA directly.

You breathe in pollution? Those particles can damage DNA too.

You’re alive? Normal metabolism generates its own DNA damage, no outside cause needed.

DNA picks up damage constantly. Researchers estimate tens of thousands of DNA lesions per cell every single day. Imagine that. Your body is quite a machine.

But your cells are not passive bystanders. Each one carries built-in repair crews. These are proteins whose entire job is to patrol the DNA, find damage and fix it before it causes trouble. Think of it less like a single alarm system and more like a maintenance team that never clocks out.

Most of the time, this works. The damage gets caught, the repair gets made and the cell moves on as if nothing happened.

This is the biological process people are usually referring to when they say we “get cancer cells every day.”

More accurately, our cells constantly accumulate DNA damage and copying mistakes. The vast majority are repaired before they ever become something more serious.

When The Safety Nets Aren’t Enough

Occasionally, though, damage slips past the repair crew. Maybe there is simply too much damage at once. Maybe one of the repair proteins isn’t working properly because of an inherited mutation, such as BRCA1 or BRCA2, among others.

When that happens, the cell has one more safety net. A protein called p53, nicknamed the guardian of the genome, acts like a checkpoint guard.

It pauses the cell before division and gives the repair machinery one more chance to fix the damage. If the damage is too severe, p53 can trigger the cell to self-destruct, a process called apoptosis. This prevents damaged DNA from being copied into the next generation of cells.

DNA repair and p53 are two of the body’s best-known safeguards against cancer. But they are only part of the story. Our cells have several overlapping quality-control systems that recognize different types of DNA damage, repair copying mistakes or eliminate cells that can no longer be trusted.

Most of the time, these systems work remarkably well together. Cancer usually develops only after enough of these protective layers begin to fail.

And that’s why I struggle with the phrase “we all have cancer cells.” Most damaged cells never become cancer in the first place. They are repaired, stopped from dividing or eliminated long before they ever reach that stage.

So, no, healthy people don’t generally walk around carrying established cancer cells. They carry cells that constantly pick up DNA damage, most of which is successfully repaired before it can become anything more. That’s a very different biological situation from having cells that have already acquired the defining characteristics of cancer.

Once Cancer Exists, The Rules Change

Everything we’ve discussed so far describes a healthy body trying to prevent cancer from developing.

But once a cell has escaped those safeguards and become cancerous, the role of DNA repair changes.

Cancer cells continue to accumulate DNA damage, often at an even faster rate than healthy cells.

In fact, they often experience even more damage because they divide rapidly, live under constant stress and have genomes that are already unstable. Yet despite all of that damage, they still need to survive.

To do so, they become heavily dependent on the DNA repair pathways they still have. Without them, many cancer cells simply couldn’t keep dividing.

This creates one of the biggest paradoxes in cancer biology. Before cancer develops, DNA repair is one of our greatest defenses. After cancer develops, those same repair systems can become one of the tumor’s greatest allies.

Why Many Cancer Treatments Damage DNA

Understanding DNA repair doesn’t just explain how healthy cells protect themselves. It also explains why many cancer treatments work.

One of the biggest ironies in oncology is that many of our most effective treatments deliberately damage DNA. Radiotherapy creates breaks in DNA. Many chemotherapy drugs interfere with DNA replication or overwhelm the cell with more damage than it can repair.

At first glance, that sounds contradictory. If DNA damage contributes to cancer, why would doctors intentionally create even more of it?

The answer is that cancer cells are often already living close to their repair limit. Years of rapid growth and accumulated damage have made them heavily dependent on the repair pathways they still possess.

Healthy cells are affected too, which is why chemotherapy and radiotherapy cause side effects. But because healthy cells generally have intact repair systems and far fewer genetic abnormalities, many are able to recover once treatment ends.

Unfortunately, not every cancer cell dies. Some survive by relying even more heavily on the repair mechanisms they still have. Others acquire additional changes that make them less sensitive to future treatment. This is why treatment resistance remains such a major challenge in oncology.

This growing understanding has also led to a different treatment strategy. Rather than simply causing more DNA damage, researchers have begun targeting the repair systems themselves.

PARP inhibitors are an example. They exploit weaknesses in cancers carrying BRCA mutations by blocking one of their remaining repair pathways, leaving the cancer cell with no effective backup while largely sparing healthy cells.

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Can We Influence These Pathways?

Integrative oncology often looks at these same pathways from a different angle.

The goal isn’t simply to “boost DNA repair.” In established cancer, that could be a double-edged sword because cancer cells rely on many of these same repair systems to survive.

Instead, integrative strategies focus on restoring the body’s normal surveillance mechanisms while increasing stress specifically within cancer cells.

Researchers also studied several natural compounds that influence the body’s DNA damage response and surveillance systems, including p53.

Preclinical studies found that melatonin and sulforaphane enhanced p53 signaling in certain cancer models. Vitamin D supported genomic stability by regulating genes involved in DNA repair, cell-cycle control and differentiation.

These pathways help damaged cells pause division, repair DNA or, when the damage is beyond repair, undergo apoptosis.

Researchers are also investigating repurposed drugs that target these pathways.

Ivermectin was reported in laboratory studies to restore or enhance p53 signaling in certain tumor models while disrupting multiple pathways cancer cells use for survival.

Mebendazole, another anti-parasitic, was investigated for complementary effects on cell division, stress responses and tumor metabolism rather than directly damaging DNA.

The goal isn’t to create damage. It’s to exploit the weaknesses cancer cells develop as they become increasingly dependent on the repair systems they have left.

That’s why many integrative clinics combine therapies. One treatment may increase stress inside the cancer cell. Another limits its ability to repair that damage or recover from it.

So Do We All Have Cancer Cells?

After all of this, let’s go back to the question we started with.

Do we all have cancer cells every day?

Not exactly.

What we all have is DNA damage. Every day, our cells accumulate damage from viruses, chronic inflammation, environmental toxins, radiation and the normal wear and tear of metabolism.

Most of that damage is repaired. Cells that cannot be repaired are often stopped from dividing or instructed to self-destruct before they ever become cancer.

That is very different from carrying established cancer cells.

As cancer patients, this has practical implications. We can monitor circulating tumor cells (CTCs) or circulating tumor DNA (ctDNA) during and after treatment. These are not simply healthy cells that picked up a bit of DNA damage. They are cells, or fragments of cells, that have already crossed the threshold into cancer biology.

A circulating tumor cell has detached from the primary tumor and entered the bloodstream. Although a small fraction can eventually seed metastases, most never do. Many will die or be eliminated by the immune system. But biologically, they are already cancer cells. That is fundamentally different from the damaged cells that exist temporarily in a healthy body before being repaired or removed.

To me, that’s why the wording matters.

Saying “we all have cancer cells” may sound like a universal truth, but it blurs the distinction between cells that have the potential to become cancer and cells that already are cancer.

Healthy cells accumulate DNA damage but remain under the body’s control. Cancer cells have already escaped the safeguards designed to prevent them from existing. Those are fundamentally different biological states.

Much of what I share comes from years of researching and making decisions during my own cancer journey. I share this as personal research and perspective for educational purposes only. Please consult your healthcare team before making treatment decisions, including decisions about supplements or medications.

References

Hanahan D. Hallmarks of Cancer: New Dimensions. Cancer Discovery. 2022.

Jackson SP, Bartek J. The DNA-damage response in human biology and disease. Nature. 2009.

Lindahl T. Instability and decay of the primary structure of DNA. Nature. 1993.

Hoeijmakers JHJ. DNA damage, aging, and cancer. New England Journal of Medicine. 2009.

Vousden KH, Lane DP. p53 in health and disease. Nature Reviews Molecular Cell Biology. 2007.

Lord CJ, Ashworth A. PARP inhibitors: Synthetic lethality in the clinic. Science. 2017.

Feldman D, Krishnan AV, Swami S, Giovannucci E, Feldman BJ. The role of vitamin D in reducing cancer risk and progression. Nature Reviews Cancer. 2014.

Reiter RJ, Rosales-Corral SA, Tan DX, et al. Melatonin as a mitochondria-targeted antioxidant: one of evolution’s best ideas. Cell Death & Disease. 2017.

Juge N, Mithen RF, Traka M. Molecular basis for chemoprevention by sulforaphane. Cell Mol Life Sci. 2007.

Juarez M, Schcolnik-Cabrera A, Dueñas-González A. The multitargeted drug ivermectin: from an antiparasitic agent to a repositioned cancer drug. American Journal of Cancer Research. 2018.

Dobrosotskaya IY, Hammer GD, Schteingart DE, Maturen KE, Worden FP. Mebendazole as a Candidate for Drug Repurposing in Oncology: An Extensive Review of Current Literature. Cancers (Basel). 2019.

Pantel K, Alix-Panabières C. Liquid biopsy and minimal residual disease—latest advances and implications for cure. Nature Reviews Clinical Oncology. 2019.

In part 1, I covered what liquid biopsies are and the two main types of material they test: circulating tumor cells (CTCs) or circulating tumor DNA (ctDNA). Those are captured from a blood sample. Some platforms may also incorporate information from a tumor tissue sample.

Before deciding which test to order, you need to know what question you want answered first.

First, I’ll be discussing the three main clinical questions that should guide your choice of liquid biopsy. Then, I’ll show how those map onto the main types of tests on the market and what information you will get.

There’s also a short list of questions worth getting answered by the integrative practitioner before you agree to any test. Future posts will go deeper into individual platforms: what each one measures, how to read them and where their limits are.

Liquid biopsies each provide different types of information and sometimes complement each other. In my opinion, they should be ordered more often than we think.

Start With The Question, Not The Test

Aside from a few select liquid biopsies, most tests are not embraced by mainstream oncology. They can usually be ordered through integrative practitioners specializing in cancer or the labs themselves.

Before ordering a liquid biopsy, three main questions need to be answered:

1. Am I in active treatment and is the tumor responding by conventional standards?

When someone has ongoing treatment, it’s possible doctors already know whether the tumor is responding or not. In such cases, it might not be necessary to do a liquid biopsy since you already have that information.

Also, at the beginning of the disease, patients are often overwhelmed with appointments and protocols. Most people don’t have time to research liquid biopsies.

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As part of the series the ABCs of Cancer Biology, we have arrived at C. Cancer stem cells, or CSCs, are a key (and unfortunate) part of cancer biology and progression.

When a tumor is gone and the scans show no evidence of disease (NED), the assumption is that the cancer is gone. However, most cancer treatments today work by eradicating fast-dividing tumor cells. But cancer stem cells are different. They are often far more resistant to conventional treatments and can survive therapy.

They are tricky residents in the body. They can hide, go dormant and then wake up one day to cause a relapse or metastasis.

Imagine a tumor as an army of soldiers. If treatment kills enough soldiers, the whole unit collapses. But a handful of officers stay back in their bunkers. They do not fight. Radar can’t see them. Their main job is to manage the army. And if one day the army is wiped out, they’re responsible for rebuilding it. These are the CSCs. They’re among the most dangerous cells in a tumor because they can rebuild it.

The Officers Of The Tumor

Most cells in a tumor are bulk cells. They divide fast and that’s what treatment targets. They die off under chemo or radiation.

CSCs sit at the top of the hierarchy. They renew themselves. They also produce every other cell type found in the tumor. Just like a human body has stem cells that can turn into any type of cell, a single CSC can, in theory, regenerate an entire tumor. Bulk cells cannot do that.

Those CSCs make up a tiny share of any tumor, often under 1%.

The idea behind CSCs dates back to 1877. A German pathologist, Julius Cohnheim, building on his mentor Rudolf Virchow’s earlier work, proposed that cancer might arise from leftover embryonic cells sitting dormant in adult tissue.

These cells could get reactivated and start growing where they shouldn’t. When he used a microscope, he found that tumor tissue often looked strikingly similar to embryonic tissue. Back then, it was not possible to test his theory. So, it remained a hypothesis and was largely ignored for over a century.

It wasn’t until 1994 that John Dick, Tsvee Lapidot and colleagues showed that only a small subset of human leukemia cells could restart the disease when transplanted into mice, while most leukemic cells could not.

In 1997, John Dick and Dominique Bonnet identified the responsible leukemia-initiating cells, marked by the CD34+/CD38− phenotype. Published in Nature Medicine, that study is widely regarded as the birth of the modern cancer stem cell concept.

Although it didn’t prove Cohnheim’s embryonal-rest hypothesis, it revived interest in the idea that tumors may be hierarchically organized around a small population of stem-like cells capable of sustaining the cancer.

It took another decade or so to determine the CSCs in solid tumors. In 2003, Muhammad Al-Hajj and colleagues at the University of Michigan identified the first solid tumor stem cells in breast cancer. They used the CD44+/CD24-low signature that’s still a standard marker set today.

Brain tumor stem cells followed in 2004. Since then, researchers have found the same hierarchy in most solid tumors: colon, pancreatic, lung and others.

Catching A Cell That Hides

So how can a patient, whether with active disease or in remission, test for CSCs?

There are labs that can test an approximation of what’s suspected to be a CSC-type cell. More sophisticated techniques are used mostly in research and sadly are not available to the general patient population.

Researchers usually combine surface markers with functional tests to determine if a tumor cell has stem-cell characteristics.

Marker-Based Testing

The main markers are CD44, CD133 and ALDH1. In breast cancer, CD44+/CD24low is the classic stem-like signature. When the enzyme ALDH1 is high, it tracks with stem-like behavior in breast and colon cancer.

Because some cells can express CD44 and not be a true CSC, or vice versa, labs use several markers. Markers can also shift over time within the same tumor, so what you’re seeing today may change in six months.

Functional Testing

The other way to identify a CSC is to test what it actually does, not just what markers it carries. That’s called a functional test. The main one is a tumorsphere assay.

Some specialized laboratories isolate circulating tumor cells from a blood sample. They then place those in a culture dish where they cannot easily attach and grow. Most tumor cells do not survive. But cells with stem-like properties can persist and form small round clusters called spheres. Researchers use this assay to enrich for and study cells with stem-like behavior, although sphere formation alone does not prove that a cell is a true CSC.

This is still a pretty niche area and only a few companies in the U.S. and Europe combined provide testing either via a conventional physician or an integrative practitioner.

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Built To Survive

Chemo and radiation target fast-dividing cells. CSCs divide slowly. That alone lets them dodge the main mechanism these treatments rely on.

They also carry built-in defenses called efflux pumps. Those pumps sit in the cell membrane. An efflux pump physically grabs chemo drugs and pumps them back out before the drug can do damage, which is another way CSCs dodge treatment that would otherwise kill them.

CSCs also keep levels of reactive oxygen species, or ROS, lower than bulk cells. This means chemo and radiation cause less permanent damage to begin with. And their repair systems run faster, so even when damage does reach them, it gets fixed quickly.

Then there’s dormancy. A dormant cell isn’t dividing at all. It’s nearly invisible to treatments built to catch cells mid-division.

Radiation runs into a related wall. It works by damaging DNA badly enough that a cell can’t repair itself and dies. CSCs, with their stronger repair systems, patch that damage before it turns fatal.

This is why CSCs tend to make up a larger share of what’s left after radiation. The bulk cells around them die off first and leave the resistant fraction standing.

A landmark 2006 glioblastoma study found the CD133+ marker enriched three to four fold in cells that survived radiation. A 2016 paper pushed back on the broader assumption though, arguing that surviving cells aren’t actually more radioresistant on their own, and that shrinking tumor volume is a misleading way to judge whether the resistant population made it through. The field hasn’t fully settled this.

So when doctors say we’ll do radiation or chemo

“to reduce your risk of it coming back,”
“to make sure they get anything left behind,”
“as a precaution,”

I find those statements difficult to hear.

It may help clear local cancer cells that are still dividing. But CSCs are often more resistant. That doesn’t mean these treatments have no benefit. Rather, CSC biology may help explain why cancer can still return despite treatment.

The tumor microenvironment, what integrative oncology focuses on, also matters for CSCs. Researchers call it the niche. It functions like life support: low oxygen, signaling from nearby stromal cells and protection from immune attack.

The niche reinforces a CSC’s stem-like state but doesn’t fully control it. A true CSC keeps some of that self-renewal capacity even outside the niche, which is what a tumorsphere assay measures.

One of the trickiest things about CSCs is that they are highly plastic. They adapt. Some non-stem cancer cells convert into stem-like cells under the right conditions. This is called epithelial-to-mesenchymal transition (EMT), where a cell loosens its grip on its neighbors and turns mobile and invasive. This can lead to relapse or metastasis.

The Comeback Nobody Wants

A tumor can shrink dramatically on imaging and the person still relapses months or years later. The bulk mass is gone. The CSCs that survived treatment are still there. Given time and the right conditions, they rebuild.

It’s something that I’ve unfortunately been tracking in real time via a liquid biopsy test I did in Germany.

My circulating tumor cells have been shifting toward a stem-like phenotype and it seems that a relapse could just be around the corner. It’s a reality that’s not pleasant to know, but I still prefer knowing it to navigating blindly. Unfortunately, science and protocols have not caught up with how to address such cases before anything shows up on scans. I am certain that in the future, this will be possible. But for now, all we can do is track.

Such evolution can also explain why recurrences can be more aggressive than the original tumor. If CSCs survived treatment because of their resistance mechanisms, the tumor that regrows is enriched for those same resistant cells. Therapy can end up selecting for exactly the cells hardest to kill next time.

Dormancy plays a role too. A CSC can sit inactive for years before something wakes it up. That’s part of why late recurrence, five years out, ten, sometimes fifteen, stays a real risk in several cancer types. That’s particularly true in hormone-driven breast cancer. It’s also why maintaining a healthy lifestyle matters beyond just the treatment phase.

Inflammation, tissue injury, hormonal shifts and changes in the surrounding microenvironment have all been proposed as triggers for waking CSCs. Even though there’s no consensus in science on this, the body’s internal environment is suggested as an active player in whether a dormant cell stays asleep or starts dividing again.

This is a separate question from what triggers non-stem cells to convert toward a stem-like state in the first place, which is the plasticity/EMT process covered earlier.

My own case looks more like plasticity than a dormant cell waking up. HER2-positive breast cancer has been shown to promote this kind of shift. So, biology itself can override the general triggers just described.

The Cracks In The Armor

So, is there any hope?

There is some. CSCs aren’t untouchable. They carry specific dependencies, and researchers are actively working to exploit them, from the signaling pathways that keep CSCs stem-like to the way they hide from the immune system, along with which specific tests and repurposed-drug combinations are worth pursuing. That’s a big topic on its own, one I’ll cover in more depth, including the integrative angle and where to access CSC-specific testing, in a follow-up piece.

As mentioned earlier, it’s a fascinating field. But for patients like me and many others, it’s incredibly frustrating. The idea behind CSCs has been around for nearly 150 years. Actual proof, and the tools to test for them, are 20 to 30 years old. Why is medicine still moving this slowly?

Shrinking a tumor was never the hard part. Reaching the small population capable of rebuilding it is.

Much of what I share comes from years of researching and making decisions during my own cancer journey. I share this as personal research and perspective for educational purposes only. Please consult your healthcare team before making treatment decisions, including decisions about supplements or medications.

References

Al-Hajj M, Wicha MS, Benito-Hernandez A, Morrison SJ, Clarke MF. Prospective identification of tumorigenic breast cancer cells. Proceedings of the National Academy of Sciences USA. 2003;100(7):3983-3988.

Bao S, Wu Q, McLendon RE, et al. Glioma stem cells promote radioresistance by preferential activation of the DNA damage response. Nature. 2006;444:756-760.

Bonnet D, Dick JE. Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nature Medicine. 1997;3:730-737.

Gerweck LE, Wakimoto H. At the crossroads of cancer stem cells, radiation biology, and radiation oncology. Cancer Research. 2016;76(5):994-998.

Lapidot T, Sirard C, Vormoor J, et al. A cell initiating human acute myeloid leukaemia after transplantation into SCID mice. Nature. 1994;367:645-648.

Reya T, Morrison SJ, Clarke MF, Weissman IL. Stem cells, cancer, and cancer stem cells. Nature. 2001;414:105-111.

Singh SK, Hawkins C, Clarke ID, et al. Identification of human brain tumour initiating cells. Nature. 2004;432:396-401.

Apigenin is a flavonoid found in parsley, celery, chamomile, oregano and some citrus fruits. Chamomile tea is one of the richest common sources.

For years it sat in the background of flavonoid research. Substances like quercetin and EGCG got more attention. This is changing now.

In the last two years alone, apigenin has shown up in reviews on breast cancer, cervical cancer, leukemia and liver cancer. A 2025 study found apigenin could suppress the harmful effects of cellular aging while improving chemotherapy response.

This piece walks through the research and the evidence behind apigenin, as well as how it can be added as an adjunct in cancer treatment.

Inside, we’re looking at the cancers where apigenin has shown the strongest effects. I am also covering how it influences cell division, metastasis and cancer stem cells. In addition, apigenin can help clear the inflammatory “zombie cells” that accumulate with aging.

Absorption remains its biggest limitation. I’m outlining what doses are commonly used in integrative care and why caution is advised depending on the subtype of breast cancer you have.

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Tumors were supposed to be sterile. No bacteria growing on them. That was the assumption for decades. Immune cells constantly patrol nearby tissue, ready to clear out anything foreign. Not exactly a welcoming spot for microbes.

Turns out that assumption was wrong. Many tumors have been found to carry bacterial communities, some sitting right on their surface. And a lot of them are not just scattered bacteria floating around. They are organized into biofilms.

Bacteria That Build Their Own Roof

Think of a biofilm as a bacterial city. The bacteria show up, settle in one spot and build a shared roof over their heads. That roof is a sticky layer made of sugars, proteins and DNA the bacteria produce themselves. Scientists call it an extracellular matrix, but “shared protective roof” gets the idea across just as well.

Once that roof is built, the bacteria underneath are much harder to kill. Antibiotics that would wipe out free-floating bacteria in minutes often cannot get through the matrix. Immune cells have the same problem. They cannot break in easily either.

You already know biofilms from everyday life, even if you never called them that. Dental plaque is a biofilm, sitting on the surface of a tooth. So is the slimy film that builds up on a catheter or a joint implant, which is exactly why those infections are so stubborn to clear. Same biology, different surface. In some cancers, that surface turns out to be the tumor itself.

The Tumors Caught Harboring Them

Colorectal cancer has the strongest evidence so far. A study out of Johns Hopkins looked at tumor tissue and found dense bacterial biofilms coating the surface layer over the tumor in 89% of right-sided colon cancers, compared with just 13% on the left side.

These were not stray bacteria that happened to land there during surgery. They were organized, sticky communities sitting directly on the tumor surface, in contact with the outermost tumor cells. One bacterium shows up again and again in these biofilms: Fusobacterium nucleatum, a species already tied to colorectal cancer through other research.

Colorectal cancer is not the only place this has turned up. Evidence for organized biofilms has also emerged in pancreatic cancer. Breast tumors have been shown to harbor bacteria, though organized surface biofilms remain much less well characterized.

A different, larger study found bacteria living inside tumor and immune cells across seven cancer types, including breast, lung and pancreatic cancer. That is a broader finding about bacteria existing within tumor tissue generally. It is not the same as an organized biofilm sitting on the surface. Both point to tumors being far less sterile than assumed, but they are two different observations.

Five Ways Biofilms Can Fuel Cancer Growth

A biofilm sitting on a tumor is not just an odd house guest. There are a few ways it could actually be pushing cancer along.

The first is inflammation. A biofilm is a foreign object the immune system cannot fully clear. So it keeps trying, over and over, releasing inflammatory signals the whole time. That kind of low-grade, chronic inflammation is already one of the best documented drivers behind cancer starting and growing in the first place. A biofilm sitting on tissue for months or years gives that fire more fuel.

The second is barrier breakdown. In the colon, biofilms strip away the protective mucus layer that normally keeps gut bacteria at a safe distance from the cells lining the intestine. Once that layer thins out, bacteria and whatever they produce sit closer to those cells, with more opportunity to cause DNA damage or trigger abnormal growth signals.

The third is more direct. Some bacteria in these biofilms make substances that damage DNA in nearby cells. Certain strains of E. coli produce a toxin called colibactin, and colibactin leaves behind a specific, recognizable pattern of DNA damage that researchers found inside colorectal tumor cells.

The fourth is telling the immune system to back off. Fusobacterium nucleatum carries a protein called Fap2. Fap2 binds to TIGIT, a receptor found on immune cells like natural killer cells and T cells. TIGIT normally acts as a brake pedal for the immune system. Fap2 pushes that pedal down, so immune cells that should be attacking the tumor get told to stand down instead. This one is not just about creating favorable conditions. It is the bacteria actively disarming the body’s own defense.

Fusobacterium nucleatum has one more trick. It carries a surface protein called FadA, which latches onto E-cadherin, the protein that normally glues epithelial cells tightly to their neighbors.

Loss of E-cadherin is one of the hallmark features of epithelial to mesenchymal transition, or EMT. This is the process where fixed, well-behaved tissue cells start acting like individual cells on the move. Tumors with these biofilms tend to have lower E-cadherin levels overall, though a direct causal link between FadA and EMT itself is not yet established. FadA binding to E-cadherin does activate a known growth signaling pathway, Wnt/beta-catenin, inside the tumor cell.

When Bacteria Help A Tumor Survive Chemo

Here is where it gets more concerning. Fusobacterium nucleatum has been linked to resistance against oxaliplatin, one of the chemotherapy drugs commonly used in colorectal cancer.

The proposed mechanism involves autophagy, which is the cell’s own recycling and survival system. Under stress, a cell can switch on autophagy to break down and reuse its own components rather than dying. Fusobacterium seems to trigger this survival switch in tumor cells, helping them survive the chemo that would otherwise kill them.

So a biofilm may not just be sitting there. If it is shielding bacteria that help tumor cells survive treatment, it could be indirectly shielding the tumor too.

The Missing Piece On Routine Pathology

Biofilms are hard to study. Standard tissue processing in a lab can knock the whole structure apart. Regular bacterial culture, growing the organism in a dish, often fails, because a lot of these bacteria do not grow well outside their biofilm home.

Most of the findings so far have come from a technique called FISH, short for fluorescence in situ hybridization. It works like a molecular flashlight: glowing probes usually target bacterial 16S rRNA sequences, so whatever carries them lights up under a microscope.

If that name sounds familiar, it should. FISH is a routine clinical test already, usually aimed at a different target, like checking HER2 in breast cancer or the ALK gene in some lung cancers. Those probes stick to human DNA, and the result lands on your pathology report.

That version isn’t standardized for clinical use. No approved probe set, no scoring system, no spot on a routine report. So if you’ve had a FISH test done, it was almost certainly for something like HER2, not bacteria.

Thinking In Terms Of Terrain

This does not prove biofilms cause cancer. It is way too early to say fixing your gut bacteria fixes a tumor.

But the pattern is hard to ignore if you already think in terms of terrain. Chronic inflammation, a weakened gut barrier, an overgrown or imbalanced microbial community: these are not new ideas in integrative practice. They tend to circle back to gut health, oral health and inflammation, the same territory a lot of terrain-focused work already pays attention to.

It does give a mechanism, though. An actual biological pathway. One reason terrain work might matter more than it gets credit for, in a model of cancer that usually stays focused on the tumor alone.

Fusobacterium nucleatum, the bacterium showing up again and again in these tumor biofilms, normally lives in the mouth. It is one of the most common bacteria in periodontal disease. For it to end up organized on a colorectal tumor, it has to travel. Most likely through the bloodstream or by being swallowed and surviving the trip through the gut. That creates a plausible biological link between oral health and colorectal cancer. An actual migration route for a specific organism.

Do Any Repurposed Drugs Target Biofilm

A few do, and some are already familiar names.

Disulfiram has shown antibiofilm activity in experimental models. One proposed mechanism is disruption of bacterial copper homeostasis after forming copper complexes.

NSAIDs have shown antibiofilm activity too. Aspirin, diclofenac and a few others reduced biofilm formation in lab studies against E. coli and Staphylococcus aureus. The likely mechanism: damage to the bacterial cell membrane, plus interference with DNA replication.

Statins and metformin show up here as adjuncts, not standalone agents. Combined with antibiotics, they enhanced activity against biofilm-forming bacteria in some studies, including tuberculosis.

None of this is specific to cancer-associated biofilms yet. Most of it comes from work on chronic wound infections, respiratory infections or drug-resistant bacteria in general. Whether any of it translates to a biofilm sitting on a colorectal tumor is still an open question.

One drug is being tested more directly, right now. A proof-of-concept trial is giving metronidazole, a common antibiotic, to colorectal cancer patients with high Fusobacterium levels before surgery, to see if it lowers the bacterial load in the tumor. The trial is still recruiting, so there are no results yet. But it’s a first step toward testing a drug directly against a cancer-associated biofilm, rather than borrowing evidence from an unrelated infection.

Tumors Were Never Supposed to Have Those

Bacteria organizing into little walled cities on the surface of a tumor is still a fairly new idea, unfamiliar to most patients and many clinicians outside research settings. But it connects to things you already know: chronic inflammation, a broken barrier, DNA damage, and now, treatment resistance. All potentially shaped by an uninvited microbial community that tumors were once assumed not to carry at all.

Much of what I share comes from years of researching and making decisions during my own cancer journey. I share this as personal research and perspective for educational purposes only. Please consult your healthcare team before making treatment decisions, including decisions about supplements or medications.

References

1. Dejea CM, et al. Microbiota organization is a distinct feature of proximal colorectal cancers. PNAS, 2014.

2. Rubinstein MR, et al. Fusobacterium nucleatum promotes colorectal carcinogenesis by modulating E-cadherin/β-catenin signaling via FadA. Cell Host & Microbe, 2013.

3. Yu T, et al. Fusobacterium nucleatum promotes chemoresistance to colorectal cancer by modulating autophagy. Cell, 2017.

4. Pleguezuelos-Manzano C, et al. Mutational signature in colorectal cancer caused by genotoxic pks+ Escherichia coli. Nature, 2020.

5. Rather IA, et al. NSAIDs as a Drug Repurposing Strategy for Biofilm Control. Frontiers in Microbiology, 2020.

6. Preoperative metronidazole treatment to evaluate its efficacy in reducing Fusobacterium nucleatum colonisation in colorectal cancer patients: a proof-of-concept trial. International Journal of Surgery, 2025.

7. Gur C, et al. Binding of the Fap2 protein of Fusobacterium nucleatum to human inhibitory receptor TIGIT protects tumors from immune cell attack. Immunity, 2015.

8. Nejman D, et al. The human tumor microbiome is composed of tumor type-specific intracellular bacteria. Science, 2020.

9. Sepich-Poore GD, et al. The microbiome and human cancer. Science, 2021.

10. Dalecki AG, et al. Disulfiram and Copper Ions Kill Mycobacterium tuberculosis in a Synergistic Manner. Antimicrobial Agents and Chemotherapy, 2015.

Integrative oncology often focuses on nutrition, exercise, supplements, sleep and stress reduction.

But there is another side to the equation that receives far less attention: whether patients have the physical, emotional and practical foundations to put that advice into practice.

It’s difficult to prepare healthy meals when you’re exhausted. To exercise when you’re overwhelmed by appointments. To meditate when you’re worried about paying for treatment. To prioritize sleep when anxiety keeps you awake.

Cancer doesn’t just challenge the body. It also dismantles many of the basics that make healthy behaviors possible. Those that healthy people often take for granted. For cancer patients, it becomes even more important, yet often challenging to achieve.

Abraham Maslow’s hierarchy of needs provides a useful framework for understanding these changes. In 1943, he proposed that human needs are organized in layers, beginning with physiological needs such as food and sleep, followed by safety, belonging, esteem and purpose.

Although developed as a psychological theory, it also provides a useful framework for understanding something cancer care rarely addresses: the invisible work patients do simply to restore the foundations of daily life.

In this post, I’m focusing on the first two because they’re often the basis that makes everything else possible.

1. Sleep: The First Foundation To Break

If one layer deserves attention before all the others, it’s sleep.

New diagnosis, scanxiety, pain, steroids, hospital schedules, night sweats and treatment side effects can all disrupt the body’s normal rhythm. What begins as a few difficult nights often becomes weeks or months of fragmented sleep.

The consequences extend beyond fatigue. Disrupted circadian rhythms and abnormal cortisol patterns have been linked to poorer outcomes in several cancers, including breast, lung, colorectal and kidney cancer. In metastatic breast cancer, women whose cortisol remained elevated into the evening had shorter survival than those whose cortisol followed a normal daily rhythm.

Cortisol doesn’t only regulate sleep. It also influences inflammation, immune signaling and tumor surveillance. Between 80% and 90% of patients experience significant fatigue during treatment. For nearly one in three, it persists long after treatment ends.

Poor sleep doesn’t cause cancer. But it removes one of the conditions the body depends on to recover and tolerate treatment as well as possible.

Looking Beyond Sleep Hygiene

Sleep isn’t determined by a single factor and so it isn’t fixed by just one either.

Here are some tips:

• Don’t think of sleep as passive rest. During sleep, the body coordinates many of its repair and maintenance processes, including immune regulation, hormone secretion, tissue repair and metabolic housekeeping. Cancer treatment places greater demands on these systems, making restorative sleep even more important.

If you’re a night owl like me, it might be difficult to shift to an earlier bedtime. What you can try instead is shift your sleep time to an earlier time by just 10 to 20 minutes every few days or even weeks. You might be surprised to find less fatigue the next day as your circadian rhythm adjusts and better aligns with your biology.

• Review your medications and supplements with sleep in mind. Steroids, endocrine therapies, beta-blockers, opioids and even some supplements can disrupt sleep architecture. EGCG and vitamin D are often better suited to the morning or early afternoon, while sleep-supportive supplements such as melatonin or L-theanine are typically taken in the evening. Stacking too many supplements at night may also be heavy for your digestive system and especially liver. The best strategy is to thoughtfully spread those out across the day.

• Think about timing, not just the intervention. Blood pressure normally drops overnight, insulin sensitivity is generally highest earlier in the day and drug metabolism changes throughout the day. As a result, when you exercise, eat or take certain therapies may matter as much as what you do. Chronobiology is becoming an increasingly important area of cancer research. Vigorous evening exercise, late-night eating and taking stimulating supplements late in the day can disrupt circadian rhythms.

• If you wake at the same time every night, don’t automatically blame anxiety. Repeated awakenings, particularly between 2 and 4 a.m., may be triggered by a nighttime drop in blood glucose, leading to a rise in cortisol and adrenaline. Rather than reaching for a bedtime snack, focus on improving blood sugar stability throughout the evening by choosing a balanced dinner with protein, healthy fats and fiber and limiting refined carbohydrates.

2. Safety: When Life Stops Feeling Secure

Safety is a particularly sensitive subject for me. Before cancer, I rarely thought about it. After cancer, I realized how much life depends on feeling that tomorrow is reasonably secure. When that foundation is shaken, it becomes much harder to focus on healing.

The practical side of cancer such as protocols, doctors and scans may be taken care of. But the harder and less visible parts for patients can be as simple as

“Who’s going to drive me to and back from chemo or surgery?”

“Will I be able to do grocery shopping and eat properly?”

“What if I’m not feeling well at home and no one is there to help me?”

These are everyday things that most people who go about their lives don’t even think about. It happens automatically. But when cancer strikes, all of a sudden this structure becomes extremely important, because your life depends on them. And your healing too.

Then there’s the financial fallout that can last not only from day one of the diagnosis but long after treatment ends.

Medical expenses add up, even with insurance. You still have regular bills to pay too. Meanwhile you’re juggling appointments and fear. You look at your savings or retirement account and realize you’ll have to tap those because those “hard times” they were for, or your “retirement piggy bank” you were counting on may suddenly become the only means of sustaining yourself.

You can also go through job loss or feel obligated to quit it because of debilitating side effects. People who are self-employed can experience an even greater loss of financial stability because there’s no safety net. Add to this all the complementary therapies and you’re dealing with an enormous strain on your nervous system and your wallet.

While the rest of the world keeps moving, all of a sudden people find themselves literally feeling like the whole structure around them has collapsed and they have to rebuild while also taking care of their health.

Research consistently shows that this “financial toxicity” is more than an economic problem. It has been associated with higher psychological distress, poorer quality of life, reduced treatment adherence and, in some studies, worse survival. Financial strain becomes another burden the body carries alongside the disease.

Safety also extends beyond money. Living alone often means every appointment, grocery trip, insurance form, medication refill and household task falls on one person. Patients with strong practical support frequently recover some of that lost bandwidth, while those without it may spend months or years carrying the entire logistical burden themselves.

Unlike many other life crises, cancer rarely has a clear endpoint. You can move from one scan to the next, one blood test to the next and one treatment decision to the next without a clear resolution point in time. That prolonged uncertainty can keep the stress response activated long after the initial diagnosis, making it difficult to relax even in remission.

Creating Islands Of Predictability

You can’t eliminate uncertainty, but you can reduce how much of your day is consumed by it. Maybe that’s even one of the hidden lessons in cancer: learning how to live with uncertainty.

I’m not saying you have to push through no matter what. The reality is that many patients don’t have the luxury of waiting until they feel ready to rebuild. And it’s the small choices that can make them feel like they’re making progress, step by step, one day at a time.

Reducing unnecessary decisions can help preserve mental energy. Simple routines such as repeating the same breakfast, planning meals for the week or keeping a regular grocery list free up cognitive bandwidth for the decisions that matter most. Try to keep the basics of your structure intact, or create a new structure that fits your new reality without making it harder for you. Make things easier and remove the superfluous stuff.

Financial uncertainty often feels less overwhelming once it is put on paper. A simple treatment budget, an overview of insurance coverage or discussing costs with your healthcare team early may help prevent unexpected financial stress later on.

Ask for help from family and friends. Sometimes you’d be surprised at who will step up, even if some may not. Appreciate those who do, those are the little angels in your life. There’s a reason the term “angel investor” is used in the financial industry. It’s someone who doesn’t need the money but who believes in the “project.” In this case, the “project” is you.

Another strategy is to separate “cancer administration” from everyday life. Try not to answer insurance emails, schedule appointments and read scan reports whenever they arrive. Instead, set aside a dedicated block each week to deal with paperwork and logistics. Containing those tasks prevents them from taking over every day.

If people ask how they can help, give them something specific. A ride to treatment, picking up groceries, preparing a meal or helping with paperwork often provides far more relief than a general offer of support.

Finally, be intentional about how much time you spend consuming cancer information. Constantly searching for new studies, treatments or patient stories can create the illusion of control while increasing anxiety. Setting boundaries around when you research cancer helps prevent it from occupying every spare moment.

Being intentional about how you spend your energy and resources might be a new skill you’ll learn. I’ve consciously cut back time with people who drain my reserves and increasingly spend time with those who add something to my life. I’ve cut down on unnecessary expenses and have prioritized all my spending on healing. This means cutting out certain vacation plans or going out to dinner when you can eat cheaper and healthier food at home. This might seem a bit sad, but I view this very differently. My life has shifted and I’m making my new normal work for me.

Who knows what the future holds? I’m taking today as the day I’m living and I’m grateful for that.

Much of what I share comes from years of researching and making decisions during my own cancer journey. I share this as personal research and perspective for educational purposes only. Please consult your healthcare team before making treatment decisions, including decisions about supplements or medications.

References:

• National Cancer Institute. Sleep Problems (PDQ®)–Patient Version. https://www.cancer.gov/about-cancer/treatment/side-effects/sleep-problems

• Sulli G, Lam MTY, Panda S. Interplay between circadian clock and cancer: New frontiers for cancer treatment. Trends in Cancer. 2019;5(8):475-494.

• Papantoniou K, et al. Circadian disruption and cancer risk: Evidence and mechanisms. Nature Reviews Cancer. 2024.

• Holt-Lunstad J, Smith TB, Baker M, Harris T, Stephenson D. Loneliness and social isolation as risk factors for mortality: A meta-analytic review. Perspectives on Psychological Science. 2015;10(2):227-237.

• Cheng S, Yi J, Pace K, et al. Impact of loneliness on cancer mortality: A systematic review and meta-analysis. BMJ Oncology. 2025;4:e000840.

• Halpern MT, Thamm C, Knowles R, Chan RJ. Cancer Survivors’ Experience of Care and Financial Toxicity: Results From a National Survey. JCO Oncology Practice. 2025.

• National Cancer Institute. Financial Toxicity (Financial Distress) and Cancer Treatment. https://www.cancer.gov/about-cancer/managing-care/track-care-costs/financial-toxicity-pdq

This second article looks at the strategies available to interfere with that process.

Both conventional and integrative medicine target angiogenesis, but they do so in very different ways.

Avastin blocks VEGF directly. Integrative therapies tend to influence multiple biological signals that encourage new blood vessel growth. Rather than shutting down a single pathway, the goal is to make the environment less favorable for the tumor.

Start With The Soil

One of the biggest misconceptions is that angiogenesis is controlled by a single molecule like VEGF.

It isn’t.

Blood vessel growth is influenced by inflammation, oxidative stress, insulin signaling, oxygen availability, immune cells and many other factors. That is the reason tumors often find ways around drugs that target only one pathway.

This is also where integrative oncology takes a different perspective.

Rather than relying on one intervention, it aims to improve the overall terrain that supports cancer growth.

Lifestyle Still Matters

Maintaining a healthy weight, improving insulin sensitivity, exercising regularly, avoiding smoking and following a plant-rich diet are all associated with a less inflammatory internal environment. Those changes affect far more than blood sugar alone. They also influence many of the chemical messengers involved in tumor biology.

Read more

When I was diagnosed with cancer, I had to teach myself the language doctors and researchers use every day. Most of it is never explained in plain terms. So I decided to make it easier for patients and caregivers trying to understand this disease.

Welcome to a new series, The ABCs of Cancer Biology.

Every week I will share a new term, working through the alphabet one letter at a time, and sometimes more than once for the same letter. Some weeks will cover a single idea. Other weeks will need a few related terms together since cancer biology rarely stays in one lane.

Let’s start with A for angiogenesis.

Here’s something that surprised me when I first learned it: a tumor cannot simply keep growing forever. In fact, without solving one very specific biological problem, most solid tumors never become much larger than the size of a pinhead.

Think of it as a tumor building its own plumbing so it can keep feeding itself. But before it can do that, it has to overcome a very basic challenge: survival.

The Wall Every Tumor Hits

A cluster of cancer cells can grow to only a few millimeters in size using nothing but the oxygen and nutrients that seep in from nearby tissue. No blood vessels needed yet. But past that size, the cells in the middle of the cluster are simply too far from any blood supply. They stop getting what they need and they start to starve.

This is the wall every solid tumor eventually hits. Not because of some flaw in its DNA. A clump of cells can only get so big before the ones in the center go hungry.

Some tumors sit at this wall for years. Doctors call this dormancy. The tumor is there, technically, but it stays small, slow and often invisible on a scan. Many tumors never make it past this stage at all.

If you have ever heard a small finding described as stable or indolent, this is often part of what’s going on underneath. The cells are present, but without their own blood supply they simply cannot grow much bigger. It is also part of why some cancers can seem to appear out of nowhere on a later scan. The tumor was not actually new. It just crossed the size where a scan could finally see it and angiogenesis is usually what got it there.

How A Starving Tumor Calls For Help

When cells run low on oxygen, they send out a distress signal, a molecule called VEGF. Think of VEGF as an SOS flare. It travels through nearby tissue until it reaches an existing blood vessel and knocks on the door.

The cells that line the inside of blood vessels pick up that signal and respond. The tumor isn’t building blood vessels itself. It’s persuading your own healthy cells to do the construction work. They start dividing, stretching and growing new branches toward the tumor, the same way your body grows new blood vessels to heal a cut. Except here, the wound never stops sending the signal.

This moment, when a tumor switches from just getting by to actively building its own supply lines, is often called the angiogenic switch. It’s a turning point. Once it happens, the tumor is no longer capped by how close it sits to existing blood vessels. It can keep growing as long as it keeps sending out the signal.

And now it is connected to the bloodstream. It doesn’t just gain oxygen and nutrients. It also gains an escape route. The same blood vessels that feed the tumor can later become the highways cancer cells use to reach distant organs.

Why The Plumbing Is A Problem, Not A Fix

The blood vessels a tumor builds are nothing like the ones the rest of your body runs on. Normal blood vessels are built in an orderly way, properly sized branches that connect smoothly. A tumor’s vessels are a mess. They’re crooked, leaky and disorganized, more like pipes thrown together in a hurry than a real plumbing system.

That messiness cuts both ways for patients. Leaky vessels are part of how cancer manages to spread. A gap in a vessel wall is an opening a cancer cell can slip through to get into the bloodstream and travel somewhere else in the body.

You would also think more blood vessels means chemotherapy reaches every part of a tumor more easily. In practice it often works the opposite way. Because the vessels are so disorganized, blood flow inside a tumor is uneven. Some areas get plenty of blood. Others barely get any, remaining starved, acidic and difficult to treat.

Ironically, tumors build blood vessels because they need oxygen, yet the vessels they create are so abnormal that many parts of the tumor remain oxygen deprived anyway. This state, known as hypoxia, doesn’t just make tumors harder to treat. It also encourages many cancers to become more aggressive. We’ll come back to that when we reach the letter H.

Where This Shows Up In Real Treatment

Because VEGF plays such a central role, it became an obvious drug target in oncology. A well known example is bevacizumab, sold as Avastin. It was approved in 2004 and is still used today, often alongside chemotherapy, across a range of cancers.

Other drugs go after the same pathway from a different angle, working inside the blood vessel cells instead of on VEGF itself. The goal is the same either way. Slow down or stop the tumor from building new supply lines.

These drugs cause side effects because VEGF isn’t a cancer-only molecule. It also helps wounds heal, keeps blood pressure steady and helps the kidneys filter properly. That’s why blocking VEGF can raise blood pressure, slow wound healing after surgery or cause protein to leak into urine.

VEGF can also be measured directly in a blood sample, usually ordered as a serum or plasma VEGF test. It is not part of routine cancer screening and most oncologists never order it. Some integrative physicians and research centers use it as one additional piece of information alongside imaging and other biomarkers.

In some U.S. states, patients can also order certain VEGF tests directly through direct-to-consumer laboratory services without first obtaining a physician’s order. Worth knowing though: some versions of this test are labeled for research use only, meaning they were not cleared or approved by the FDA for clinical diagnostic use. That does not make the result meaningless. It just means it is meant to be read alongside other information rather than on its own.

A single VEGF result rarely tells the whole story. Looking at trends over months alongside imaging and other laboratory markers is usually much more informative.

Higher VEGF levels can suggest that blood vessel formation is more active, but they cannot tell you why. A growing tumor is one possibility. Normal healing is another. A normal VEGF level does not rule cancer out either. Like many biomarkers, VEGF is one thread in a much larger biological story.

The Biggest Misconception

The idea is simple. Cut off the blood supply, starve the tumor, watch it die. That’s roughly how these drugs were pitched when they were new. It isn’t entirely wrong, but it’s incomplete.

Blocking VEGF doesn’t wipe out a tumor’s blood vessels. It prunes them. The weakest, leakiest vessels tend to disappear first, while the ones that survive can actually work better — a strange effect researchers call vascular normalization. For a while that can make chemotherapy work more effectively rather than less, part of why these drugs are usually paired with chemo instead of used alone.

Blood isn’t the only thing a tumor knows how to hijack, however. Some tumors simply latch onto blood vessels that are already there instead of building new ones. Others find ways to move blood through channels made from their own cells, skipping the VEGF signal completely. Both are part of why tumors can eventually find a way around anti-VEGF drugs.

None of this makes VEGF any less important. It just means angiogenesis isn’t a switch you can permanently flip off. It’s more like a supply chain. Cut off one vendor and a resourceful tumor will look for another.

That is not a reason to write off anti-VEGF treatment. It is a reason these drugs tend to work best as one piece of a bigger plan rather than a single silver bullet. Understanding that difference is the whole point of learning the biology in the first place.

Angiogenesis is only the beginning. As you’ll see throughout this series, cancer doesn’t invent new biology. It repeatedly hijacks the biology that normally keeps us alive.

Once you start seeing that pattern, cancer begins to make a lot more sense.

Building its own blood supply is only half the survival problem a tumor has to solve. Avoiding its own death solves another, which is why we’re staying on the letter A for one more week.

Much of what I share comes from years of researching and making decisions during my own cancer journey. I share this as personal research and perspective for educational purposes only. Please consult your healthcare team before making treatment decisions, including decisions about supplements or medications.

References

Ferrara N, Hillan KJ, Gerber HP, Novotny W. Discovery and development of bevacizumab, an anti-VEGF antibody for treating cancer. Nature Reviews Drug Discovery, 2004.

Jain RK. Normalization of tumor vasculature: an emerging concept in antiangiogenic therapy. Science, 2005.

Muz B, de la Puente P, Azab F, Azab AK. The role of hypoxia in cancer progression, angiogenesis, metastasis, and resistance to therapy. Hypoxia, 2015.

U.S. Food and Drug Administration. Approval history for Avastin (bevacizumab) in metastatic colorectal cancer, with later approvals across additional cancer types. FDA Approval History, 2004.

Quest Diagnostics. Vascular Endothelial Growth Factor (VEGF), ELISA, listed for research use only. Quest Diagnostics Test Directory, 2026.

If you’ve had cancer, chances are you’ve come across tumor markers with names like CA 15-3, CEA, CA-125, CA 19-9 or PSA. For some patients these numbers become a source of reassurance. For others they become a source of anxiety. Every change is scrutinized. Is treatment working? Is the disease progressing? Has the cancer returned?

Many oncologists don’t routinely order tumor markers after treatment. Others use them regularly in patients with advanced disease. Patients are left wondering: if these tests can detect cancer, why aren’t they used more often? And if they’re not reliable why use them at all?

The truth lies somewhere in between. Tumor markers are neither crystal balls nor meaningless numbers. Understanding what they can and cannot tell you is often more useful than the number itself.

What Is a Tumor Marker?

A tumor marker is a substance measured in the blood that may be associated with the presence or activity of certain cancers. Most are proteins produced by cancer cells. Some can also be released by normal tissue, or by the body reacting to inflammation or tissue damage.

Tumor markers do not directly measure the amount of cancer in the body. Instead, they provide an indirect signal that may reflect tumor activity. Whether that signal is meaningful depends on the cancer type, its biology, the amount of disease present and the individual patient’s physiology.

Even cancers in the same organ don’t all produce the same marker. Some release large amounts into the bloodstream. Others produce little or none.

This is why they need to be considered alongside imaging, pathology, symptoms, physical examination and clinical history.

Two Different Jobs: Detecting Cancer vs Tracking It

One reason tumor markers cause so much confusion is that their usefulness changes with the stage of cancer.

In early-stage disease, the question is usually whether cancer has come back. Many recurrences are simply too small to produce a measurable amount of marker. False-positive elevations are common. This limits how useful markers are as a routine surveillance tool for a lot of patients.

Once metastatic disease is already present, the question changes. Doctors already know the cancer is there. What they want to know is whether treatment is shrinking it, holding it steady or letting it progress.

Metastases usually mean more cancer cells release tumor markers into the bloodstream. That’s why changes are often easier to see than with small, early-stage tumors.

This is where these markers become much more useful. Doctors look at them alongside scans and how the patient is doing. A rising marker may prompt a scan sooner than planned. A falling marker can be reassuring.

CEA: A Marker Shared by Many Cancers

CEA, or carcinoembryonic antigen, was one of the first tumor markers introduced into clinical practice.

CEA isn’t specific to one cancer. It can rise in colorectal, pancreatic, gastric, lung and some breast cancers. It is often markedly elevated in medullary thyroid cancer, a rarer type that starts in a different tissue altogether.

Smoking is the most common cause of a mildly elevated CEA in someone without cancer. Liver disease and inflammatory bowel disease can do the same. Mild elevations (roughly 5-15 ng/mL) are often non-cancerous, whereas much higher or steadily rising values carry more weight.

Not every tumor produces CEA. Some colorectal cancers, for example, never produce it. This is why doctors check a baseline CEA before treatment starts. That initial value helps determine whether CEA is likely to be a useful marker for that particular patient. If it’s already low or normal at diagnosis, it usually isn’t a reliable marker to follow afterward.

CA 15-3 and CA 27.29: The Breast Cancer Markers

CA 15-3 measures a fragment of MUC1, a protein found on the surface of many breast cancer cells and shed into the bloodstream. It was first identified in the early 1980s and became one of the most widely used breast cancer markers by the end of that decade.

The marker tends to stay low in early-stage breast cancer and rise with more advanced disease. Here too, it is more useful for tracking known metastatic disease than for catching an early recurrence.

Its usefulness also depends on the biology of the tumor itself.

HER2-positive breast cancers tend to produce less of the protein CA 15-3 measures, so this marker can understate active disease in that subtype. Triple negative breast cancer is more unpredictable, some tumors still produce plenty of the marker and others don’t, so it shouldn’t be assumed to behave one way across the board.

CA 27.29 measures a different piece of the same underlying protein as CA 15-3. It was developed a few years later, in the early 1990s, as a more standardized version of the same test. The two provide very similar clinical information, but they shouldn’t be alternated when following trends because the assays are calibrated differently.

CA-125: Best Known in Ovarian Cancer

CA-125 was discovered in 1981 and the 35 U/mL cutoff still used today comes from that original research.

It works best in women with epithelial ovarian cancer, especially the more common serous subtype. In these cases, it often rises and falls with the amount of cancer present, making it useful for monitoring treatment.

Not every ovarian cancer subtype behaves the same way. Clear cell and mucinous ovarian cancers tend to produce less CA-125 than the more common serous type, even though both carry a worse prognosis. A normal CA-125 in a woman with one of these subtypes should not be viewed as reassuring on its own. A low result may reflect the biology of the tumor rather than the absence of disease.

CA-125 also rises with plenty of non-cancerous conditions: endometriosis, fibroids, pelvic infection, menstruation, pregnancy and recent abdominal surgery among them. This overlap is large enough in premenopausal women that an elevated result carries limited weight by itself. It becomes more meaningful after menopause, once most of those benign causes become less likely.

PSA: Useful and Widely Misunderstood

PSA was first characterized in 1979. The key thing to understand about it is that it’s prostate specific, not cancer specific: both normal and cancerous prostate tissue produce it.

Because the prostate naturally grows with age, what counts as normal PSA also rises with age. Younger men are held to a lower threshold than men in their seventies.

PSA can rise for many reasons: an enlarged prostate, infection, recent ejaculation, cycling and even certain medical procedures. One elevated reading usually leads to a repeat test rather than an immediate biopsy.

In men already diagnosed with prostate cancer, PSA becomes much more informative. Doctors watch how fast it rises over time rather than any single number, since a steady, gradual rise means something different than a sudden jump.

CA 19-9: Pancreatic and Biliary Cancers, With a Genetic Catch

CA 19-9 was isolated in 1979 and later became the main blood marker used for pancreatic cancer.

Very high readings, well into the thousands, are associated with disease that has spread too far to operate on. A falling CA 19-9 during chemotherapy is generally a good sign.

Its biggest limitation isn’t the cancer, it’s genetics. Around 5% to 10% of people can’t produce CA 19-9 at all, regardless of how advanced their cancer is, because they lack a specific blood group marker needed to make it. In those people, CA 19-9 stays normal no matter what the disease is doing, so a normal result doesn’t rule anything out.

CA 19-9 also rises sharply with a blocked bile duct, gallstones or pancreatitis, none of which are cancer. A falling CA 19-9 after a blocked duct is cleared may simply reflect that fix rather than the cancer responding to treatment, so it’s worth waiting until other liver values normalize before reading too much into the trend.

Patterns Matter More Than Single Numbers

One of the most common mistakes patients make is focusing on a single lab value.

Take a CA 15-3 that rises from 18 to 20 U/mL. Is that meaningful? In most cases, probably not. Every lab test has some normal biological and analytical variation built into it. Small fluctuations are expected and often mean little.

Now if the same marker goes from 18 to 26, then to 39, then to 58 over several months, that’s a different story. Whether it turns out to be recurrent disease, inflammation or something else still needs investigation. But the trend itself deserves attention.

The opposite happens too. Patients sometimes panic over a temporary rise that later settles back to baseline. Occasionally, tumor markers rise briefly after treatment starts before falling again. This temporary increase doesn’t necessarily mean treatment isn’t working. Labs can also show slight analytical and biological variability.

Whenever possible, trends should be read using the same lab and the same assay. Different labs can use different testing methods, which makes direct comparison less reliable.

Why Some Oncologists Skip Markers Entirely

It can be surprising to learn that some oncologists rarely order tumor markers after someone finishes treatment for early-stage cancer. If the test exists, it’s natural to wonder why not just use it.

The reasoning comes down to evidence, and preference. For many early-stage cancers, routine marker monitoring hasn’t been shown to help people live longer, even when it catches a rise before symptoms appear. Detecting a change earlier doesn’t automatically translate into a better outcome if there’s nothing yet to act on.

There’s also a real cost to false positives. An unexplained marker rise often leads to more scans, more blood draws, more appointments and weeks of uncertainty. This can be financially taxing without necessarily leading to actionable disease.

Oncologists who monitor markers closely and those who don’t are usually weighing the same tradeoff differently: earlier warning against unnecessary anxiety and testing. Tumor markers remain one tool among several, not the final word.

Tumor Markers Aren’t a General Cancer Screening Test

One limitation of traditional tumor markers is that they apply to only a relatively small number of cancers. Even within those cancers, many tumors produce little or none of the marker, particularly in early-stage disease. This means there is no blood panel that can reliably screen the body for “cancer” as a whole.

As a result, many people look for broader screening options. Today, private whole-body MRI scans and multi-cancer early detection (MCED) blood tests are becoming increasingly available. Unlike tumor markers used to monitor known cancer, these tests aim to detect previously undiagnosed cancers in otherwise healthy or asymptomatic individuals.

These technologies are promising, but they also have important limitations. Whole-body MRI can detect incidental findings that ultimately prove harmless yet still lead to additional scans, biopsies and anxiety.

Multi-cancer blood tests may miss early cancers or detect a signal without identifying exactly where the cancer is located. At present, none of these approaches has replaced guideline-based screening or become a universal standard for the general population.

For selected high-risk individuals, they may represent another option to discuss with a physician. Like tumor markers, however, they are additional tools rather than definitive answers. Cost also can be a deciding factor.

Where Newer Blood Tests Fit In

Liquid biopsies are increasingly used, with several now FDA approved for certain cancers and in specific clinical settings. Some are also reimbursed by private insurance and even Medicare.

Circulating tumor DNA (ctDNA) and circulating tumor cell (CTC) testing provide information that traditional protein tumor markers cannot. ctDNA looks for fragments of tumor DNA circulating in the bloodstream.

CTC testing identifies whole tumor cells. Depending on the platform, these tests can also assess tumor mutations, phenotypes and sometimes sensitivity to therapies, repurposed drugs or nutraceuticals.

Liquid biopsies are not the same as—and are not a replacement for—CA 15-3, CEA, CA-125, PSA, or CA 19-9. They generally provide far more detailed molecular information, but they have not yet replaced traditional tumor markers in routine oncology practice.

I do believe they will gradually become more integrated into medical practice because they offer insights that extend well beyond conventional tumor markers and may even help inform treatment decisions.

Today, these tests can often be ordered through integrative oncology clinics, functional medicine practitioners, and sometimes by contacting the testing companies directly.

If you’d like to learn more about liquid biopsies, see my previous article here. I’ll also be covering them in much greater detail in future posts, as they deserve a far more in-depth discussion than I could include here. Here too, cost can influence the decision.

The Bottom Line

A normal tumor marker does not guarantee cancer is absent. An elevated marker does not automatically mean cancer has returned.

The same CA 15-3 result carries different weight in a patient who finished treatment for early-stage disease than in a patient with known metastases. The same CEA can be reassuring in one person and concerning in another depending on the trend, the imaging and the tumor’s own biology.

Knowing a marker’s strengths, limitations and blind spots won’t remove uncertainty, but it can replace false reassurance—or unnecessary fear—with a clearer understanding of what the result is, and isn’t, telling you.

Much of what I share comes from years of researching and making decisions during my own cancer journey. I share this as personal research and perspective for educational purposes only. Please consult your healthcare team before making treatment decisions, including decisions about supplements or medications.

References

1. Kallioniemi OP, Oksa H, Aaran RK, Hietanen T, Lehtinen M, Koivula T. Serum CA 15-3 assay in the diagnosis and follow-up of breast cancer. Br J Cancer. 1988.

2. De Cock T et al. CA 15-3 and metastatic breast cancer detection, cited in Medscape emedicine overview of CA 15-3.

3. Gold P, Freedman SO. Demonstration of tumor-specific antigens in human colonic carcinomata. J Exp Med. 1965.

4. Thangavelu A et al. False-positive elevations of carcinoembryonic antigen in patients with a history of resected colorectal cancer. PMC.

5. Bast RC Jr, Klug TL, St John E, et al. A radioimmunoassay using a monoclonal antibody to monitor the course of epithelial ovarian cancer. N Engl J Med. 1983.

6. Vergote I et al. CA-125 in mucinous and clear cell epithelial ovarian cancer, Gynecologic Oncology Group analysis. PMC.

7. Chu TM, Wang MC. Purification and characterization of prostate specific antigen. 1979.

8. PSA velocity and reference range study in Japanese men. PMC, 2023.

9. Koprowski H, Steplewski Z, Mitchell K, Herlyn M, Herlyn D, Fuhrer P. Colorectal carcinoma antigens detected by hybridoma antibodies. Somatic Cell Genet. 1979.

10. Luo G et al. Carbohydrate antigen 19-9, tumor marker: past, present and future. World J Gastroenterol. PMC.

Resveratrol is a compound found naturally in red grape skins, red wine and a handful of other plants, though most supplements on the market are extracted from Japanese knotweed rather than grapes. It’s been studied for decades as a possible anti-cancer compound, with real mechanistic evidence behind that reputation in several cancer types.

In Part 1, I covered where resveratrol’s anti-cancer reputation holds up. Colorectal, pancreatic and lung cancer all showed a compound with mostly favorable effects against cancer. But once hormones enter the picture, things become considerably more complicated.

Breast and prostate cancer together account for more new cancer diagnoses worldwide each year than any other cancer type. That scale is part of why the hormone receptor question matters so much.

A very large number of people diagnosed with one of these cancers will eventually come across resveratrol, whether through supplements, online discussions or recommendations from others.

I’ve met many women who were advised to take resveratrol because of its anti-cancer reputation. Unfortunately, that recommendation isn’t nearly as straightforward as it sounds.

In approximately 70–75% of breast cancers, estrogen signaling is one of the main drivers of tumor growth. In prostate cancer, it’s primarily androgens such as testosterone that promote growth. Unlike the cancers discussed in Part 1, resveratrol doesn’t just affect inflammation, oxidative stress and apoptosis. It can also bind directly to hormone receptors themselves, creating an additional layer of complexity.

None of the mechanisms from Part 1 disappear here. Resveratrol’s anti-cancer effects still operate in breast and prostate tissue. But hormone receptors add another, less predictable layer on top of them.

That direct receptor interaction also means the numbers coming out of laboratory studies need translating before they mean much to someone deciding whether to take a supplement. Whether those laboratory concentrations can be reached in the human body makes a very big difference.

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Resveratrol shows up on almost every “anti-cancer supplement” list. Red wine, grapes and headlines about cancer prevention going back two decades. It’s the kind of ingredient people add to their routine without a second thought.

What doesn’t show up on those lists is that resveratrol’s effects depend entirely on whether it’s used for longevity, general health, anti-cancer potential or as an adjunct to cancer treatment. Its risk-benefit profile also changes depending on the cancer type and dose.

There’s more research behind this compound than most patients realize. Some of it is reassuring. Some of it isn’t. In one clinical trial, resveratrol caused serious harm. In another, it did nothing concerning at all. Same compound, different outcome. That is the thread running through this entire article.

And it’s exactly why I think blanket supplement advice is so unhelpful in oncology. “Anti-cancer” is rarely the whole story.

Why Resveratrol Became Famous

Resveratrol is a compound plants make when they’re under attack. Grape skins produce it in response to fungal infection and UV stress. It occurs naturally in red wine, grapes, peanuts and blueberries.

But the plant most supplement manufacturers actually extract it from isn’t the grape. It’s Japanese knotweed, or Reynoutria japonica (formerly Polygonum cuspidatum), an invasive plant that happens to be a much richer and cheaper source. Most bottles labeled “resveratrol” on a supplement shelf trace back to knotweed root, not wine country.

Resveratrol owes its fame to a nutrition mystery from the 1990s known as the French paradox.

Researchers noticed that people in France ate a diet high in saturated fat yet had comparatively low rates of heart disease. Red wine consumption became one of the leading theories for why.

Resveratrol was singled out as the likely protective ingredient in that wine. That single association launched decades of research into everything else resveratrol might do, including cancer. That was long before cancer-specific data existed to support those hopes.

Most people encounter resveratrol long before any cancer diagnosis.

It’s a fixture in the anti-aging supplement world. That reputation comes from research on longevity pathways, particularly the sirtuins, the same pathways thought to be activated by calorie restriction in animal studies.

It also appears in heart health supplements because of research on blood vessel function and cholesterol. Skincare brands use it as an antioxidant ingredient in serums and creams.

None of that general-population research was designed with active cancer in mind. A dose that seems reasonable for cardiovascular health or skin aging doesn’t automatically translate to oncology.

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Since being diagnosed with cancer, I have made integrative cancer support part of my strategy. It has been quite a road, with ups and downs, and a steep learning curve. On several occasions, advocating for my own care has made a real difference to my outcomes.

But there are also observations and lessons that have come out of this experience. And I’d like to share those because information is power, especially in cancer.

Having visited several integrative cancer clinics, I have seen approaches that made biological sense and others that did not. Cancer is unforgiving when mistakes are made.

That’s why it’s so important to select a functional or integrative practitioner who truly understands cancer.

When Good Intentions Are Not Enough

Let me start with some examples.

I have met well-intentioned practitioners and even doctors who prescribe folate as a blanket supplement to cancer patients. To all of them! That doesn’t mean folate is never appropriate. It means it shouldn’t be prescribed automatically without considering the patient’s situation.

I have been in clinics that administer high-dose vitamin C for months on end without verifying results, without tracking oxidative stress or monitoring cancer behavior. They didn’t have any specific strategy for these patients. What they were doing is selling the products and tools they had, at the detriment of many patients.

I have met others who prescribe B12 or other mitochondrial stimulants to cancer patients without a second thought. Vitamin B12 is essential for DNA synthesis and cell division. Because rapidly dividing cells also require these processes, blanket supplementation in cancer patients deserves more thought than that.

I have also met patients who trusted these practitioners because that was all they knew. Some rejected conventional treatment without knowing they had options that were not overly toxic or invasive. They believed that what they were receiving would save them. Often it didn’t.

Just as poor practice exists in conventional medicine, it exists in integrative care too. Some intentions are good. Some practitioners simply do not know better. Some are motivated more by selling protocols than by individualizing care.

Cancer patients are often frightened and exhausted when they seek integrative care. That vulnerability is part of why poor practice in this space causes so much damage. Time is not a resource cancer patients can afford to waste. And trust placed in the wrong hands can cost more than money.

So here is an honest account of how I think patients need to approach integrative care when navigating cancer. I am absolutely in favor of nutraceuticals, repurposed drugs and adjunct therapies.

But the critical questions are when, how much, for how long and in which situation. These are not secondary details. For cancer patients, they can mean regression or progression. Healing or declining.

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Why Cancer Is Its Own Field

Not every practitioner who understands nutrition, supplements or functional medicine also understands tumor biology. That is not a criticism. Cancer plays by its own biological rules and demands an equally individualized approach.

Functional and integrative medicine is built on a powerful framework: find what is dysregulated, support what is depleted, reduce what is excessive. For metabolic disorders, autoimmunity or chronic fatigue, that approach is genuinely powerful.

Cancer cells are not waiting to be restored. They have rewritten the rules around their own survival.

They evolve under pressure, develop resistance, manipulate their local immune environment and suppress recognition from the inside.

They recruit blood vessels to feed themselves. They shed circulating tumor cells capable of reaching distant organs, where a small fraction may eventually establish metastases if conditions are favorable.

They shift how they produce energy depending on what is available. They can lose surface markers, undergo epithelial-to-mesenchymal transition and interact with the surrounding microenvironment in ways that are still being uncovered.

A practitioner who understands the body deeply does not automatically understand any of that.

This is also why oncology itself has become so specialized. Even medical oncologists focus on specific tumor types, because no single person can master every aspect of cancer. The same principle applies to integrative care.

Where The Gaps Show Up

One of the signs that someone understands cancer biology is how they think about oxidative stress.

In general functional medicine, oxidative stress is broadly the enemy. Antioxidants are protective. That is true enough for healthy people.

In cancer, it depends entirely on context. Some chemotherapy drugs work by generating reactive oxygen species (ROS) inside tumor cells. High-dose antioxidants given at the wrong moment may blunt that effect. The same substance that protects healthy tissue can interfere with treatment in another context. A cancer-literate practitioner asks what the treatment mechanism is before recommending anything. They do not apply a blanket antioxidant protocol during active treatment.

The same precision applies to what feeds cancer. Most practitioners have heard that sugar feeds cancer. That is a simplification that can mislead. What cancer actually exploits is metabolic flexibility: glucose, glutamine, fatty acids, depending on the tumor type and environment. A practitioner working from an incomplete metabolic map, restricting glucose while overlooking other metabolic pathways, may be missing more than they realize.

Then there is resistance. This is where many integrative approaches fall short in ways that are not obvious at first.

Resistance is not unique to chemotherapy. Cancer cells can develop resistance to natural substances through the same mechanisms: upregulating efflux pumps, activating compensatory pathways, shifting metabolic phenotype.

A practitioner who understands resistance does not automatically assume that a natural substance should be continued indefinitely simply because it is natural. The biology does not care whether a treatment is pharmaceutical or botanical.

Specific things that can go wrong

Some of the most problematic recommendations come from practitioners with genuine expertise, applied without cancer-specific knowledge.

High-dose antioxidants during chemotherapy or radiotherapy. NAC, oral high-dose vitamin C and certain polyphenols at high doses may warrant caution depending on the treatment mechanism. Timing and dose matter in ways that a general antioxidant framework does not capture.

Plant estrogens in hormone-sensitive cancers. Resveratrol and certain isoflavones have anti-inflammatory profiles in healthy populations. In ER-positive breast cancer or other hormone-driven tumors, their interaction with hormone signaling can require specific evaluation, not a standard recommendation.

Iron supplementation for fatigue. Functional medicine commonly addresses treatment-related fatigue with iron repletion. In cancer, iron metabolism is entangled with tumor biology. Ferritin can reflect inflammatory and tumor activity. Supplementing without understanding that context should not be the automatic default.

Generic fasting protocols. Fasting has genuine evidence in oncology. But protocols designed for metabolic health or longevity are not automatically appropriate during active treatment, in patients with muscle loss risk or in specific tumor types. The detail matters enormously.

What Cancer-Literate Support Actually Looks Like

It is not about credentials or titles. A physician, a naturopath, a researcher or a clinical consultant can all have genuine cancer literacy. Or not. The letters after a name tell you less than you might expect.

I have met physicians with decades of oncology experience who remained remarkably humble and curious. I have also met non-physicians who had spent years immersed in cancer biology and developed a serious understanding of the literature. And I have encountered practitioners from multiple backgrounds who relied almost entirely on marketing language instead of evidence.

Curiosity matters more than certainty.

In today’s medical environment, patients are often their own best advocates. And sometimes, their own best judges. Cancer is one of the most complex diseases we know. But patients who live with it, research it and track it daily can develop a level of familiarity with their own disease that surprises even experienced practitioners.

I have experienced this firsthand. I once worked with a naturopath I found really impressive. She was rigorous, curious and incredibly thorough. But as we reviewed my pathology, bloodwork and liquid biopsy results together, it became clear that cancer biology was not her area of expertise.

We ended up discussing papers and mechanisms that she hadn’t encountered before. At one point she told me she didn’t feel comfortable charging me anymore because she felt she was learning as much from our discussions as I was from her.

By that point I had spent nearly every day for years reading about my own cancer subtype.

That moment showed real professional integrity. She recognized where the limits of her expertise were and she was honest about them. That is exactly the kind of humility I now look for in a practitioner.

Questions Worth Asking

Before/when working with an integrative practitioner in a cancer context, these questions are important to get answers to.

1. How much of their practice is dedicated specifically to cancer patients?

2. Can they explain the biological reasoning behind their recommendation?

3. Have they actually reviewed your pathology report?

4. Do they adapt protocols based on cancer subtype, biomarkers and current treatment?

5. How do they stay up to date with cancer research?

6. How do they think about interactions between supplements and treatments?

7. What would make them change course in their strategy?

8. What are the biggest uncertainties in your situation?

9. What are their goals with this recommendation: symptom management, reducing side effects, metabolic support, immune support or directly targeting cancer biology?

10. If they could only recommend three interventions for your case, what would they be and why?

How To Approach This In Practice

I understand that reading a list of questions off to a new practitioner is not how a real appointment works. What I do instead is focus on three that reveal the most, fast.

What is your overall strategy for my cancer? Then listen carefully to the answer. Does the practitioner discuss the particulars of your cancer, the stage and the treatment phase you are in? Is your recent bloodwork reviewed, or are additional tests ordered before anything is recommended? And when those results come back, are they actually examined in detail, or do they just sit in a portal while the protocol continues unchanged?

Why are you suggesting these specific interventions, and can you explain the biological rationale? If they say “because you are low in this” or “because most cancer patients are deficient in that,” that is a red flag. The question is not whether you are low in something. The question is whether supplementing it makes biological sense in a cancer context, for your cancer, at this stage.

How will you track results over time? Any serious protocol should have a monitoring component. If there is no plan to measure outcomes, it becomes difficult to know whether the strategy is actually working. There is only a product being sold.

And do not underestimate your gut feeling. If a protocol feels generic, if the recommendations came too fast, if the price tag does not match the level of individual attention you received, pay attention to that. You do not have to decide in the room. Sit with the information. Research it yourself. Come back with follow-up questions and see how those are received too.

I am sharing this because I learned it the hard way. If this article puts you ahead of where I was, it has done its job.

Much of what I share comes from years of researching and making decisions during my own cancer journey. I share this as personal research and perspective for educational purposes only. Please consult your healthcare team before making treatment decisions, including decisions about supplements or medications.

There is a peptide that has been approved in more than 35 countries, evaluated in over 80 clinical trials and used as an adjunct in cancer therapy for two decades.

It was isolated in the 1970s from thymus tissue and has one of the cleanest safety records in clinical peptide research. It works through mechanisms that oncologists are increasingly interested in. Yet despite that history, many cancer patients have never heard of it.

That peptide is thymosin alpha-1, abbreviated TA1 or Tα1.

Its relevance lies in the immune system.

One of the hallmarks of cancer is its ability to evade immune detection. Before a tumor becomes visible on a scan, cancer cells have often already found ways to escape the body’s surveillance mechanisms. Many tumors then go on to suppress immune function further, making it harder for the immune system to recognize and eliminate them.

Whether someone has active disease or is in remission, the question is ultimately the same: can immune surveillance be strengthened again?

Much of the interest in TA1 stems from its potential role in addressing that question.

What Exactly is TA1?

The thymus gland sits behind the sternum and is the organ responsible for producing mature T cells.

Allan Goldstein and colleagues at the Albert Einstein College of Medicine isolated thymosin alpha-1 from thymus tissue in the 1970s after identifying it as the most biologically active component of a larger thymic peptide fraction.

The synthetic form, called thymalfasin, is marketed as Zadaxin. It is approved in more than 35 countries for chronic hepatitis B, chronic hepatitis C and as an immune adjunct in cancer therapy. In the US it remains unapproved, though it has been granted orphan drug status for hepatocellular carcinoma and studied in several US-based trials.

The thymus does not stay active for life. It begins to shrink after puberty at roughly 3% per year, and by age 50 its output is a fraction of what it produced in youth. This decline contributes to immunosenescence, the gradual weakening of immune function that comes with aging. It is accelerated by chemotherapy, radiation and disease.

TA1 was developed with the idea of restoring what the shrinking thymus no longer provides.

Before we continue, a quick note.

Researching and writing articles like this takes many hours of reading studies, reviewing clinical data and speaking with clinics and practitioners. If you find value in this work and would like to support independent cancer research and education, I would be grateful for your support as a paid subscriber.

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If you’ve been diagnosed with cancer and you’re taking a daily multivitamin, there’s a near-certain ingredient inside it that your oncologist has almost certainly never mentioned: folic acid. It’s B9. The nutrient behind pregnancy health campaigns and neural tube defect prevention. The one added to flour, cereals, fortified orange juice, protein bars. The one that sounds definitively safe, even virtuous, to be taking.

It isn’t universally safe. Not for everyone. And especially not for people with an existing tumor.

For more than a decade, preclinical and clinical research has been building a case that high-dose folic acid supplementation may do exactly the opposite of what a cancer patient hopes. Not protect healthy cells but accelerate the growth of established tumors. Most patients never hear about it. Their supplement labels don’t mention it. The “it’s just a B vitamin” framing discourages the kind of scrutiny that any other compound with this data profile would automatically receive.

To understand why, it's important to distinguish folic acid from folate. Folate is the naturally occurring form of vitamin B9 found in foods, while folic acid is the synthetic form used in supplements and food fortification.

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The Folate Paradox

At dietary levels and in the context of cancer prevention in healthy cells, folate is genuinely protective. Its role is to supply the one-carbon units that cells need for DNA synthesis and repair. When folate is deficient, DNA-strand breaks accumulate, chromosomal instability rises and mutations are more likely to take hold. Low folate status is associated with increased risk of multiple cancers. This is well-established and not under dispute.

The problem begins when there is already a tumor in the picture.

Once a precancerous or cancerous cell is established, the same one-carbon machinery that supports healthy DNA repair now serves a different master. Rapidly dividing tumor cells depend heavily on folate to keep replicating. Supply more folate and you are providing a resource to the very cells you’re trying to kill.

Researchers have described this as a double-edged sword: folate preventing cancer initiation in normal cells while potentially promoting the progression of tumors that are already there. So the timing matters.

Folate and Folic Acid Are Not the Same Thing

There is another layer to this: folic acid, the form in virtually every supplement and all fortified food, is not the same thing as the folate found naturally in leafy greens and legumes.

Synthetic folic acid is biologically inactive. It has to be converted through a multi-step enzymatic process before it can be used by cells, with the rate-limiting step depending on an enzyme called DHFR (dihydrofolate reductase). When the dose is high or when DHFR is slow, folic acid backs up in the bloodstream as unmetabolized folic acid, or UMFA. UMFA appears in plasma after supplemental doses as low as 200 to 400 mcg, amounts contained in a single standard multivitamin.

Several studies have reported associations between circulating unmetabolized folic acid and reduced natural killer cell activity. NK cells are part of the immune system’s first line of cancer surveillance.

Roughly 10 to 15% of people carry a homozygous MTHFR variant, reducing their ability to convert synthetic folic acid into its active form. As a result, unmetabolized folic acid may accumulate more readily despite adequate or even high intake.

When Vitamins Collide With Treatment

For patients in active treatment, there is a second and more immediate concern: interference with antifolate chemotherapy.

Methotrexate is one of the oldest and most widely used cancer drugs still in the formulary. It works by blocking DHFR, which starves tumor cells of the folate metabolites they need to synthesize DNA.

The interaction between folate metabolism and chemotherapy is complex. Antifolate drugs such as methotrexate intentionally disrupt folate-dependent pathways, which is why folic acid supplementation requires careful management during treatment.

Research reviewing folate and antifolate interactions found that while higher folate status may reduce some treatment-related toxicities, it may simultaneously support tumor growth and protect cancer cells from the very treatment being delivered.

The Bigger Lesson

Folic acid illustrates a recurring theme in oncology: context matters. A compound that is protective in one setting can become problematic in another. The mistake is assuming that safety automatically carries over from prevention to treatment. It doesn’t.

Folic acid isn’t marketed as a cancer supplement. It shows up in prenatal vitamins, breakfast cereals and protein bars. That invisibility is precisely why it deserves more scrutiny than it currently receives.

What the Research Shows

For prostate cancer, several studies have linked folic acid supplementation and higher circulating folate levels with increased risk.

For colorectal cancer, the relationship appears to be highly dependent on timing: folate deficiency may increase the risk of tumor initiation, while supplemental folic acid may promote the growth of established lesions.

In breast cancer, animal studies found that folic acid supplementation at 2.5 to 5 times the daily requirement accelerated mammary tumor growth, with folate receptor alpha overexpression proposed as a contributing mechanism.

In liver cancer, experimental studies have shown that high-folate diets can promote tumor development through alterations in methionine metabolism and increased MAT2A expression.

A 2024 umbrella review of systematic reviews concluded that while inadequate folate status may increase cancer risk, the effects of high-dose folic acid supplementation are more complex and may be unfavorable in certain settings, particularly once neoplastic lesions are already established.

What Should Cancer Patients Actually Do?

First, don’t panic and throw out every folate-containing food in your kitchen. Natural folate from leafy greens, legumes and vegetables is not the concern. The focus here is supplemental folic acid and fortified foods.

If you take a multivitamin, B-complex or energy supplement, check the label. Many contain 400 mcg or more of folic acid. Fortified foods can add substantially to that total, particularly cereals, protein bars, meal replacement shakes and enriched grain products.

This matters even more depending on where you live. Mandatory folic acid fortification has been in place in the United States, Canada and Australia for decades. The UK introduced new regulations in 2024 requiring folic acid to be added to non-wholemeal wheat flour, with mandatory implementation by the end of 2026.

Most continental European countries do not require fortification, meaning background exposure is generally lower.

If you have a documented folate deficiency, supplementation may still be appropriate. Forms such as L-methylfolate (5-MTHF) and folinic acid avoid the issue of unmetabolized folic acid, although they do not completely resolve the question of whether additional folate may benefit an existing tumor.

If you’re curious about your folate status, RBC folate provides a better picture of long-term folate stores than standard serum folate testing. Neither test measures unmetabolized folic acid (UMFA), the form discussed throughout this article.

When cancer is already present, the question changes from preventing mutations to feeding rapidly dividing cells. What helps prevent cancer is not always the same thing that helps treat it.

Much of what I share comes from years of researching and making decisions during my own cancer journey. I share this as personal research and perspective for educational purposes only. Please consult your healthcare team before making treatment decisions, including decisions about supplements or medications.

References:

1. Troen AM, Mitchell B, Sorensen B, et al. Unmetabolized folic acid in plasma is associated with reduced natural killer cell cytotoxicity among postmenopausal women. Journal of Nutrition. 2006;136(1):189-194.

2. Kim YI. Folate: A magic bullet or a double-edged sword for colorectal cancer prevention? Gut. 2006;55(10):1387-1389.

3. Manshadi MD, Ishiguro L, Sohn KJ, et al. Folic acid supplementation promotes mammary tumor progression in a rat model. PLOS ONE. 2014;9(1):e84635.

4. Cao Y, Li X, Shi P, et al. Folate metabolism and its role in cancer progression and therapy. Signal Transduction and Targeted Therapy. 2022;7:266.

5. Thabet MA, Elmahdy M, Abdelhamid A, et al. Folate supplementation and cancer risk: A systematic review and meta-analysis. Journal of International Medical Research. 2024.

6. Umbrella review of systematic reviews examining folate status, folic acid supplementation and cancer outcomes. Journal of Global Health. 2024.

There is a weed that has been growing wild for centuries. People have been using it as medicine for over 2,000 years. It ended up in a randomized controlled trial at a major cancer center. And it helped children on chemotherapy keep their livers functional enough to stay on full treatment doses.

It is not a secret compound. It is not expensive. You can buy it at any supplement store.

It is milk thistle.

The Medicine Is In The Seeds

Milk thistle is the common name for a plant called Silybum marianum. The medicine is in the seeds. What gets extracted from those seeds is called silymarin, which is not a single molecule but a family of related compounds that work together.

The most important one is called silybin, sometimes written silibinin. It makes up the majority of the extract and carries most of the biological punch. When a supplement label says standardized silymarin, silybin is the active ingredient you are actually paying for.

Silybin has a strong relationship with liver tissue. After absorption, much of it is routed back through the liver again and again, exposing liver cells to higher concentrations than many other tissues.

The liver is where most of the interesting action happens.

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What It Does to a Stressed Liver

The liver is a processing plant. Everything you swallow gets filtered through it, including chemotherapy drugs. That processing generates harmful byproducts. Under enough chemical stress, liver cells start breaking down.

When that happens, your doctor sees it in your blood work. AST and ALT, two liver enzymes, climb above normal range. It is the liver’s way of signaling that cells are damaged and leaking. In serious cases, treatment has to be paused or doses reduced.

Silymarin works against this at several points simultaneously.

It neutralizes the harmful molecules that form during drug processing before they can damage cells. It reinforces cell walls so liver cells are harder to penetrate in the first place. It dials down inflammation inside the liver, which compounds damage if left unchecked. And it supports repair and regeneration once damage has already occurred.

Think of it as working on offense and defense at the same time. Prevention on one side, recovery on the other.

This is also why it has been used historically for toxic exposures far more dramatic than chemotherapy. In parts of Europe, intravenous silybin is part of standard emergency protocols for Amanita phalloides poisoning, otherwise known as death cap mushroom. The mushroom destroys liver cells rapidly. Silybin is given to help stop it. That is not a folk remedy. It is protocol.

When the Liver Is Struggling for Other Reasons

Fatty liver disease is quietly epidemic. A significant portion of the general population has it, and many cancer patients arrive at diagnosis already carrying some degree of liver stress before treatment even begins.

Fatty liver happens when fat accumulates inside liver cells, triggering oxidative stress, inflammation and eventually scarring if the process goes on long enough. Silymarin addresses all three of those drivers directly. It reduces oxidative stress, calms inflammation, and has documented anti-fibrotic effects, meaning it may reduce fibrotic signaling and improve some fibrosis-related markers.

The same logic applies to elevated liver enzymes from medication side effects, from past alcohol use or from causes that are not entirely clear. Silymarin has a consistent track record of bringing AST and ALT down. Most people see measurable changes within eight to twelve weeks of daily use.

There is also a specific use case that does not get enough attention: iron overload. Patients who have had many blood transfusions can accumulate excess iron, which is toxic to the liver and other organs over time. Silymarin has shown real utility here, mainly in beta-thalassemia patients receiving transfusions and standard chelation, supporting the process of clearing excess iron from the body.

There Is More to the Story Than the Liver

The liver protection story is well established. But silybin does things beyond the liver that are worth knowing about.

Radiation to the head and neck causes mouth sores. Radiation to the chest or breast causes skin burns. Both of these are painful, debilitating and can interrupt treatment. Silymarin has shown benefit for both.

For mouth sores, it is taken as a swallowed capsule at standard doses, around 420 mg per day, not applied directly to the mouth. For skin burns, a silymarin-based gel is applied topically to the affected area. These are not its most famous uses but they are real ones.

There is also early evidence for protection against damage to the kidneys from certain chemotherapy drugs, and preclinical evidence against early heart damage from doxorubicin, one of the most commonly used drugs in cancer treatment.

The pattern you start to see is a compound that protects healthy tissue from chemical and radiation insult broadly, not just in one organ.

What It Does Inside Cancer Cells

This is where things get interesting.

In laboratory studies and animal models, silybin does not just protect healthy cells. It goes after cancer cells directly. It slows cell division. It blocks signals cancer cells use to survive. It pushes cells toward programmed death, a process cancer cells are very good at evading.

It has been shown to inhibit a protein called STAT3 in preclinical models. STAT3 is active in many cancer types and closely tied to poor outcomes and resistance to treatment. Blocking STAT3 is something a lot of drug developers are trying to do with expensive compounds. Silybin appears to affect this pathway too.

It also suppresses NF-kB, a master switch for inflammation that cancer cells exploit to stay alive. And it reduces the ability of tumors to build their own blood supply, a process called angiogenesis that is essential for tumor growth beyond a certain size.

One detail that keeps appearing across these studies: the effects seem selective.

Silybin harms cancer cells while leaving healthy cells largely alone. That selectivity, if it holds in humans, is exactly what you want from any anticancer compound.

None of this is clinical evidence in humans. But this is serious mechanistic research studied across many cancer types, pointing consistently in the same direction.

Silybin appears to interfere with several of the traits that make cancer dangerous in the first place: the ability to ignore death signals, hijack inflammation, build new blood vessels and resist treatment. Whether that translates into meaningful clinical outcomes remains to be proven. But patients who take milk thistle for liver protection are getting a compound that is doing far more than protecting the liver.

The Estrogen Question

Anyone who researches milk thistle will run into warnings about estrogen. The concern is real but routinely overstated.

Silymarin interacts with estrogen receptors. There are two main types. Estrogen receptor alpha drives cell growth in breast tissue. Estrogen receptor beta tends to suppress it. Silymarin has a stronger pull toward receptor beta. In practice, activating beta can work against the growth signals that alpha drives.

Animal studies showed lower rates of mammary cancer in female rats given milk thistle, not higher. Cell studies showed silybin inducing death in ER-positive breast cancer cells. No human clinical trial has found measurable estrogenic effects from silymarin.

Major cancer centers still list caution for people with hormone-sensitive cancers and that caution is appropriate. The interaction with hormonal therapy has not been studied closely enough to rule out in either direction.

Why the Label Does Not Tell the Whole Story

Standard milk thistle supplements have an absorption problem. Silymarin does not dissolve well in water, which makes it hard for the gut to take up efficiently. Standard forms absorb somewhere between 20% and 50% of a dose, and effective blood levels can be lower still.

The solution is a formulation called silybin-phosphatidylcholine, which binds silybin to a fat molecule that the gut handles much more easily. One study found this form, in an oily softgel formulation, reached blood levels nearly 10 times higher than standard silymarin tablets at the same dose. It is sold under names like Siliphos and is widely available.

The standard dose used in most of the liver research is 420 to 840 mg of silymarin extract per day, split across two or three doses with meals. With the phosphatidylcholine form, effective doses run lower, typically 240 to 360 mg per day, because so much more of it actually reaches the bloodstream. If you are comparing products, the absorption difference is worth factoring in.

However, integrative practitioners often use substantially higher amounts, particularly when supporting liver function during intensive treatment protocols. Doses of 600–1,200 mg daily are common in integrative oncology and some clinicians use even higher amounts in selected patients.

While milk thistle has an excellent safety record, evidence supporting these higher doses is largely based on clinical experience rather than large randomized trials.

Hiding in Plain Sight

Two thousand years of medicinal use. Molecular-level research across multiple cancer types. Consistent clinical signals for lowering liver enzymes, including in chemotherapy-related liver stress. A safety record that virtually no drug can come close to matching.

For a patient going through liver-toxic treatment and watching their enzyme numbers, this is worth knowing about.

For someone dealing with fatty liver, elevated enzymes from medication or iron accumulation from transfusions, the evidence is solid enough to take seriously. The doses used in most of the liver enzyme research run between 420 and 840 mg of standardized silymarin extract per day, split across meals, over eight to twelve weeks.

The fact that it sits on a shelf next to detox teas is a marketing thing, not a science thing. The science has been there for a long time.

The Evidence Behind Milk Thistle

The most cited evidence for liver protection during chemotherapy comes from a randomized controlled trial at Columbia University, in children with acute lymphoblastic leukemia. Silymarin significantly lowered liver enzyme levels and showed a trend toward fewer children needing their chemotherapy dose cut due to liver damage. No side effects were reported.

A review of four randomized trials in children found consistent liver enzyme improvements across all four.

For fatty liver, two separate meta-analyses, one covering 26 trials and more than 2,000 patients, found significant reductions in liver enzymes, improvements in liver fat on ultrasound, and anti-scarring signals.

For radiation-related skin burns in breast cancer patients, a randomized trial found topical silymarin gel reduced severity. For mouth sores from radiation in head and neck cancer, oral silymarin reduced severity in another trial.

For the anticancer mechanisms, the evidence is preclinical, meaning laboratory and animal studies. The STAT3 and NF-kB findings are consistent across multiple cancer types and research groups. Human trials for direct anticancer effects have not yet been done at scale.

On estrogen, Memorial Sloan Kettering documents both the estrogenic activity and its preference for receptor beta, which suppresses rather than promotes cell growth.

Perhaps the most interesting thing about milk thistle is not that it works.

It is that it was working long before anyone knew why.

Modern medicine tends to trust a compound only after its mechanisms are mapped, its pathways identified, and its effects measured in trials. Milk thistle took the opposite route. People used it for centuries first. The science came later.

Sometimes the question is not whether a remedy has evidence. It is whether we have taken the time to look.

Much of what I share comes from years of researching and making decisions during my own cancer journey. I share this as personal research and perspective for educational purposes only. Please consult your healthcare team before making treatment decisions, including decisions about supplements or medications.

I have no affiliations with supplement brands or manufacturers mentioned in this article.

References

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2. National Cancer Institute. Milk Thistle (PDQ). Cancer.gov. Updated 2022.

3. CAM-Cancer Collaboration. Milk thistle (Silybum marianum). Updated June 2025.

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5. Koltai T, Fliegel L. Role of Silymarin in Cancer Treatment. Journal of Evidence-Based Integrative Medicine. 2022.

6. Shi P et al. Administration of silymarin in NAFLD/NASH: A systematic review and meta-analysis. Annals of Hepatology. 2023.

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8. Karbasforooshan H et al. Topical silymarin for prevention of acute radiodermatitis in breast cancer patients. Phytotherapy Research. 2019;33(2):379-386.

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10. Memorial Sloan Kettering Cancer Center. Milk Thistle integrative medicine monograph. MSKCC.org.

11. Won DH et al. In vitro and in vivo anti-cancer activity of silymarin on oral cancer. Oncology Research. 2018.

12. Mirhashemi SH et al. Effect of 8 weeks milk thistle supplementation on fatty liver disease in bariatric surgery candidates. Metabolism Open. 2022.

13. Hassanein EHM et al. Silymarin in pediatric acute lymphoblastic leukemia: randomized clinical evidence on hepatoprotection during chemotherapy. Frontiers in Pharmacology. 2024.