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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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!
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Come back next week for the latest information on cancer vaccines.
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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.