Chapter 94
Cancer — 21
The story of the prevention for breast cancer has some common threads with the use of finasteride (versus placebo) for prevention of prostate cancer, a drug that lowers the levels of dihydrotestosterone. Way back in 2003, a randomized trial in nearly nineteen thousand men, aged fifty-five years and older, showed a 25 percent reduction over a seven-year follow-up period. Later, in analysis that linked the participants in that trial to their Medicare claims, which extended the follow-up period to sixteen years, and subsequently to the National Death Index, which produced a median follow-up of 18.4 years, there was persistent evidence of a 25 percent reduction, but the number of deaths was small (only ninety-eight in the nearly nineteen-thousand-men cohort) and no longer statistically significant. A systematic review of eight randomized trials found a 30 percent reduction for finasteride, but the prostate cancers in the finasteride group were of higher malignant grade. That may be due to the drug’s marked lowering of prostate-specific antigen results, delaying the diagnosis. But this remains an unsettled issue, with no guidelines recommending finasteride to prevent prostate cancer.
Here again, we have ways to define the high risk of prostate cancer, such as multiancestry polygenic risk scores and many other layers of data, but we’re not using them. It certainly remains possible that finasteride, let alone other drugs, would provide important benefit for prevention if it were tested in a high-risk population rather than just using age as the sole criterion.
These examples provide marked contrast to successful cancer prevention when there is high specificity and efficacy, such as the benefits of human papilloma vaccination (HPV) to prevent cervical cancer, hepatitis B vaccination to prevent liver cancer, or prophylactic mastectomy surgery for people with BRCA mutations. Obviously, once we determine the infectious agent or the gene mutation widely, we are quite capable of moving on to a far more refined approach.
Why aren’t we routinely assessing body-wide inflammation and building on the success of anti-inflammatory drugs such as the interleukin-1β drug that significantly reduced fatal cancers and lung cancer in a large randomized trial? Why aren’t we aggressively tackling air pollution, which is unquestionably promoting cancer? We have a working blueprint for preventing so much cancer but ignoring many extraordinary opportunities in front of us.
While we need to revamp our approaches to cancer across the board—screening, accuracy of diagnosis, use of novel molecular diagnostics, treatment, and prevention—now, it will take years before we see the requisite updated changes in guidelines and routine medical practice for all things cancer related. At the population level, we cannot eke out many years of healthy aging without applying the remarkable progress we’ve made in our knowledge base. But this chapter, at the individual level, offers an anchor for your decisions, and your family members.
Part 2 has been about the big killers as measured by human lives lost. But when is a life lost exactly? What if we lose our minds in the second half of our lives?