Things that Every Cancer Patient Should Know, but Most Don’t
Learn how to take control of your care and improve your outcomes
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A new Nature study has uncovered something important: respiratory infections like influenza and COVID-19 can reawaken dormant cancer cells in the lungs, raising the risk of relapse after remission.
Here’s how it works: infection triggers inflammation, especially the cytokine IL-6, which creates a “wake-up call” for sleeping cancer cells to start dividing again.
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So where do vaccines fit in?
✅ Vaccines prevent infection (the trigger for relapse).
✅ Vaccines reduce severity if you do get sick, meaning less inflammation.
✅ Vaccines don’t generate the same prolonged inflammatory storm that infections do.The bottom line: flu and COVID vaccines aren’t just about preventing severe illness — they may also help lower the risk of dormant cancer cells being reactivated.
💡 For cancer patients and survivors, avoiding infections is a powerful way to protect health on multiple fronts.
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Even low alcohol consumption can fuel breast cancer, according to an article published in Am. Association of Cancer Research, Cancer Epidemiology, Biomarkers & Prevention.
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A recent study found breast cancer had the largest increase in alcohol-related cancer rates among women: from 6.6 → 8.1 cases per 100,000.
Out of 297,790 new U.S. breast cancer cases, an estimated 18,463 are caused by alcohol.
Shockingly, nearly 5,000 of those cases come from women who drink at low levels.
There is no truly “safe” level of alcohol when it comes to breast cancer risk.
Knowledge is power. The more we understand the risks, the more informed our choices can be.
Read the research: https://doi.org/10.1158/1055-9965.EPI-25-0243
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Metformin is often discussed as a potential anti-cancer therapy, and while its glucose-lowering effects make it biologically compelling, the research shows it doesn’t work for most cancer patients. Cancer thrives on glucose, so the idea of reducing glucose makes sense. Preclinical studies showed promise, but large clinical trials haven’t demonstrated broad benefits—except for a specific group of HER2+ breast cancer patients with a c-allele expression on their ATM gene.
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Exciting Findings for HER2+ Patients with a C-allele on the ATM Gene
A phase III randomized, placebo-controlled, double-blind trial (the “gold standard” of research) conducted across Canada, Switzerland, the US, and UK revealed:
🟢 Progression-Free Survival: Improved from 1.74 to 3.48 per 100 patient-years
🟢 Overall Survival: Reduced deaths from 1.96 to 0.69 per 100 patient-years
These results align with earlier phase II findings from a similarly designed study, but despite this robust data, there’s still no policy change to recommend metformin for these patients. Why? The trial conclusion calls for another phase III trial for confirmation.
💸 Here’s the problem: Funding another phase III trial could take years and millions. There may never be another trial, and if not, patients might never benefit from the millions already spent.
🩺 What I’m Doing
As a HER2+ mBC patient, I’m asking my oncologist if I have the C-allele, and if so, I’ll advocate for metformin. To me, this level of evidence is enough to make a decision.
🤔 What About You?
Do you think patients should decide when there’s enough evidence? Should promising findings disappear while waiting for more trials? Let’s discuss!
📩 If you find posts like this helpful, subscribe to my newsletter for more actionable strategies.Read the Research:
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Every day, your body creates millions of abnormal cells. Fortunately, your immune system is designed to find and eliminate these threats before they turn into cancer. But when cancer does take hold, it often means the immune system either didn’t recognize the danger or was unable to respond effectively.
That’s where cancer vaccines come in.
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These groundbreaking therapies are designed to train your immune system to detect and destroy cancer cells—even those that have already taken root or could reappear after treatment. Unlike traditional vaccines that prevent infections, many cancer vaccines are therapeutic: they are administered to people who have already had cancer to reduce the risk of recurrence.
In a recent episode of the Outperform Cancer podcast, we sat down with Dr. Nora Disis, Director of the Cancer Vaccine Institute and Editor-in-Chief of JAMA Oncology, to discuss what might be the most promising anti-cancer strategy yet.
According to Dr. Disis, "Cancer vaccines are most effective when a patient has no evidence of disease but is still at high risk for recurrence. That’s when the immune system is most likely to mount a strong and targeted attack."
In other words, the best time to consider a cancer vaccine may be when you're in remission.
The results emerging from cancer vaccine clinical trials are nothing short of extraordinary:
Breast Cancer: In a Phase I trial at the University of Washington, 85% of patients were still alive 10+ years after receiving a HER2-targeted DNA vaccine. Read more
Kidney Cancer: A Dana-Farber/Yale study reported that 100% of patients with advanced kidney cancer remained cancer-free more than three years after receiving a personalized vaccine. Read more
Ovarian Cancer: In another trial, 50% of patients lived 8+ years after treatment with a DNA vaccine targeting the follicle-stimulating hormone receptor. Read more
And that’s just the beginning. Cancer vaccine trials are also showing promising results in melanoma, non-small cell lung cancer, prostate, pancreatic, bladder, and more.
If you or a loved one has experienced cancer, there may be a clinical trial open right now that could help prevent it from coming back. There are currently over 100 cancer vaccine trials recruiting participants across the United States. Many are targeting patients who are in remission but at risk of recurrence. Dr. Disis emphasized that patients should not think of clinical trials as a last resort.
How to Get Involved
Visit clinicaltrials.gov and search for "cancer vaccine" with your cancer type.
Talk to your oncologist about whether you’re eligible for an ongoing trial.
Sign up for the Outperform Cancer newsletter to be notified when our full interview with Dr. Disis drops and to stay informed about the latest research.
If there's one anti-cancer strategy not to miss, this is it.
Cancer vaccines are not science fiction. They are here, they are safe, and in many cases, they are working.
Now is the time to learn more, ask questions, and explore whether a cancer vaccine might be right for you.
Be sure to stay updated on groundbreaking research and future episodes by following the Outperform Cancer podcast.
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It's important for cancer patients to receive alprazolam (Xanax) instead of lorazepam (Ativan). The anti-anxiety drug lorazepam is "correlated with significantly worse overall survival in prostate, ovarian, head and neck, uterine, colon, and breast cancer, as well as melanoma, with effects ranging from a 25% increased risk to a 116% increased risk," according to the American Association for Cancer Research.
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I couldn’t believe these numbers, and yet I know that some cancer patients are still being prescribed lorazapam (Ativan) instead of alprazolam (Xanax). I understand that “more research is necessary” to fully understand the difference in survival, but since they both provide anxiety relief, why on earth wouldn’t everyone make the shift immediately? There appears to be only upside to making the change.
The article also cites pancreatic cancer research.“Patients who took alprazolam (Xanax) had a 62% lower risk of disease progression or death compared with those who did not take alprazolam (42 patients). Conversely, patients taking lorazepam (Ativan) had a 3.83-fold higher risk of disease progression or death than patients who did not take lorazepam (29 patients).
Researchers also believe they know why lorazepam is associated with worse overall survival. Lorazepam appears to increase inflammation in the tumor microenvironment. Inflammation then leads to increased tumor growth. Alternatively, alprazolam appears to decrease the expression of the cytokine IL-6, which in turn, reduces inflammation in the tumor microenvironment. So, while lorazepam increases inflammation, alprazolam decreases inflammation.
We know that inflammation is a critical factor in tumor growth and researchers have investigated regular use of non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin and ibuprofen as a potential anti-cancer strategy. So far, research has not been conclusive, however, I’m not sure the studies have been designed to really identify the potential benefits. I’ve reached out to Dana Farber about their recent Phase II trial with aspirin which was closed early due to a lack of positive results but they have not been very forthcoming with information. I was told that they hope to provide further analysis of their data, but I wouldn’t hold your breath.
In the meantime, cancer patients are generally encouraged to look for ways to reduce inflammation. That includes systemic inflammation that can benefit from healthy diet (see gut microbiome) and exercise (see exercise as medicine) as well as making choices that influence the tumor microenvironment such as using alprazolam (Xanax) and not lorazepam (Ativan) for anxiety.
If you have questions, please send me an email.
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When we hear the term “second opinion,” it can feel like a challenge to our doctor’s expertise—a signal of doubt, mistrust, or dissatisfaction.
But what if we could reframe this entirely? Instead of focusing on a second opinion, let’s think about assembling more bright minds to tackle our medical case.
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🤝 Here’s the idea: Collaboration fuels better outcomes.
A study from the Institute for Corporate Productivity (i4cp) and Babson College found that companies promoting collaboration were 5x more likely to be high-performing. Similarly, a Stanford study revealed that the perception of working collectively boosted task persistence by 64%, increased engagement, reduced fatigue, and even improved success rates—benefits that lasted for weeks!💡 Imagine what could happen if we applied that same principle to cancer care. Instead of framing it as “questioning” your doctor, let’s build a super-collaborative care team—a network of bright minds brainstorming together for fresh ideas and better solutions.
💪 Let’s Outperform Cancer by embracing collaboration, not just opinions. Because when more people think about your case, extraordinary breakthroughs can happen.
Who’s ready to reframe the conversation? Let’s build the care teams we deserve. ❤️
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This chart is ugly in more ways than one, but I have to share it and I hope you will help me spread the word. Women diagnosed within 5-10 years of childbirth, defined as postpartum breast cancer (PPBC), have poorer prognosis compared to age, stage, and biologic subtype-matched nulliparous patients.
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This chart is ugly in more ways than one, but I have to share it and I hope you will help me spread the word. Women diagnosed within 5-10 years of childbirth, defined as postpartum breast cancer (PPBC), have poorer prognosis compared to age, stage, and biologic subtype-matched nulliparous patients. Women who are diagnosed with breast cancer within 5 years of having a child are at significant risk for future metastatic disease, and with lower overall survival rates, especially if they were diagnosed with early stage disease (stage 1 or 2).
A nulliparous young woman has a 3.3 times better chance of surviving a stage I diagnosis than her young mother counterpart. ER+ PPBC patients have a 40% likelihood of metastasis by year 15. These negative outcomes are specific to PPBC and are not found in breast cancer diagnosed during pregnancy.
Breast cancer diagnosed shortly after weaning specifically adds to the poor prognosis. They believe it is associated with postlactational involution which is the process following weaning when the mammary gland undergoes massive cell death and tissue remodeling as it returns to the pre-pregnant state.
45% of women 45 years or younger diagnosed with breast cancer are PPBC patients. With this knowledge, PPBC women should be demanding more active screening for longer periods of time.
Many recurrences, like mine, are 10-15 years after initial diagnosis. That may mean an annual MRI, ultrasounds, or perhaps ctDNA testing as it becomes more reliable. For 13 years, I met with my oncologist annually...I don’t see how a conversation and physical examination is an effective way to identify metastasis. It certainly wasn’t effective for me. I wish I had known these stats and that someone had encouraged me to demand more testing.
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Cancer Stem Cells are the cells that maintain tumor growth. Most chemotherapies will not kill CSCs because CSCs are slow growing and chemo targets fast-growing cells. There are some adjunct strategies that can kill CSCs.
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Before I started my own research, I had never heard of cancer stem cells, yet they’re central to disease-free survival. Cancer stem cells (CSCs) are a small group of cells within tumors that can cause tumor initiation and relapses. CSCs have the ability to self-renew, differentiate, and cause tumors. They can multiply indefinitely and are resistant to chemotherapy. Yes, most chemotherapies will not kill CSCs because CSCs are slow growing and chemo targets fast-growing cells. So, not surprisingly, they are thought to be responsible for relapse after therapy.
CSCs are differentiated from the cancer-initiating cell, or the cell-of-origin of cancer, which is the normal cell that receives the first cancer-causing mutations. CSCs are the cells that maintain tumor growth. At the point of tumor initiation, CSCs originate from either differentiated cells or adult tissue resident stem cells.Importantly, there are some adjunct strategies that can kill CSCs. Sulforaphane is one strategy that shows promise as a cancer stem cell killer, but there are others. It seems to me it should be an important part of any anti-cancer plan to find a way to target these annoyingly persistent cells.
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Patients had significantly better results when given multiple chemotherapy drugs at one time (combination therapy). It’s impertive to have your cancer sequenced.
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In the late 1960’s, there was a major discovery in cancer care; patients had significantly better results when given multiple chemotherapy drugs at one time (combination therapy) versus treating patients with one drug. The rationale for combination therapy is to use drugs that work by different mechanisms, thereby decreasing the likelihood that resistant cancer cells will develop. The curative regimen bleomycin/vinblastine/cisplatin for testicular cancer is an example of combination chemotherapy. This strategy makes sense to me. Cancer is complex.
To eliminate cancer completely, it seems logical that we would need to cut-off all pathways for growth. As we better understand cancer biology, we are finally making some great strides in thwarting the disease. However, each persons biology is unique. That’s why it’s imperative to get your tumor sequenced. Without the biologic information, we’re guessing which strategies will cut off the multiple pathways that cancer utilizes. When you’re newly diagnosed, and at every new recurrence, know your specific mutations and find out as much information as possible about exactly how the cancer is growing.
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Limiting fatty acid synthesis reduces HER2+ breast cancer brain growth.
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I believe that if you’re a HER2+ breast cancer patient with brain mets, you may want to know about research suggesting that limiting fatty acid synthesis reduces HER2+ breast cancer brain growth. And you may also want to understand that fatty acid synthesis is (1) rate limited by glucagon and epinephrine and (2) stimulated by insulin (insulin spikes with sugar/simple carbohydrates AND when we don’t get enough sleep insulin becomes dysregulated).
Let’s go another step further. Glucagon is stimulated by low blood sugar (glucose), protein-rich meals and adrenaline. The release of glucagon is prevented by raised blood sugar (glucose) and carbohydrate in meals.
So, patients may want to try to help their drugs work better by combining a low sugar diet with some adrenaline-including practices like daily cold plunge or sprinting during your workouts. Heck, you could even watch scary movies.