(Originally published at Scientific American, guest blog, June 26)
I had a very strange week. While in Washington, D.C., writing news releases for the Model Organisms to Human Biology: Cancer Genetics meeting sponsored by the Genetics Society of America, I had left, back home in upstate New York, my dear hospice patient. Ruth was nearing the end of her battle with liver cancer. It was jarring to go from holding her hand to listening to litanies of deranged signal transduction pathways and cascades of mutations that cause the damn diseases.
I’ve been Ruth’s hospice volunteer for 4 months, visiting her in a nursing home. Age 85 and fiercely intelligent, she refused a surgery that she knew she would likely not awaken from. So she decided to let nature take its course. Until about 3 weeks ago, it was easy to pretend she wasn’t really sick, she was so vibrant, chatty, and eager to talk about books and films and what was happening in the world. But then, suddenly, she couldn’t find the words for things. It escalated quickly. And we both knew that the large tumor in her abdomen had sent seeds of itself upward, into her brain. At least I was able to show her in my anatomy and physiology textbook that her Wernicke’s area was affected, the speech center in her cerebral cortex, and not anything vital. Yet.
So on June 17, at the opening keynote talk at the Model Organisms meeting, I felt a stab when Bert Vogelstein said, “about 3,000 resistant cells are present in every visible metastasis.” Dr. Vogelstein, whose name is practically synonymous with “genes behind colon cancer,” is director of the Ludwig Center at Johns Hopkins University and Investigator, Howard Hughes Medical Institute. He’d just shown two photos from a recent study of a melanoma patient before and soon after a new treatment: the lesions spotting his body had vanished. But after the 3,000-cell comment, Dr. Vogelstein put up a third slide – the man’s skin tumors were back. And it had taken mere months.
I thought of Ruth, and the trajectory that her cancer cells had taken from her liver to her brain.
Dr. Vogelstein continued, “Metastasis is a fait accompli. All we’re doing is killing the tumors that don’t have resistant cells. It is a side effect of the evolution of cancer,” referring to the genetic changes that drive a cancer to invade and then spread.
If even the tiniest secondary tumor harbors thousands of cells protecting it from the drugs we throw at it, what’s a cancer patient to do? Dr. Vogelstein had two suggestions: treat when the tumor is small and less likely to have acquired mutations in resistance genes, or use combinations of agents. “The chance that a single cell in a metastasis has 2 genes mutant that can confer resistance is exponentially less than they’d have one,” he said, adding that using combinations of treatments is nothing new.
One in three of us has had or will have cancer. I lost both parents to cancer, and had it myself. I think about it a lot.
If Dr. Vogelstein’s message could be summed up in one word, it would be FRUSTRATION. So here are 4 things to prevent cancer, catch it early, or keep it from spreading. The first three are so oft-stated and so obvious and time-tested I won’t even link to anything:
1. Stay away from the obvious triggers, if you can. Smoke. Sun. Pollution.
2. Eat mostly vegetables, limiting saturated fats and simple carbs.
4. Stay ahead of your doctors. Don’t get medical information from a 2-minute story on the evening news, a 10-minute visit with a health care practitioner, or blogs that repeat information (even news releases) without linking to original, peer-reviewed sources.
Educate yourself. Scan eurekalert for a heads up on breaking medical news. Check out www.clinicaltrials.gov to learn about experimental treatments. And read medical journals. Yes you can!
Medical journals run editorials, summaries, and abstracts for those who don’t want to plow through jargony, stat-studded articles. Thanks to reading back-to-back studies in the New England Journal of Medicine, in March 2009, someone close to me chose active surveillance instead of surgery for prostate cancer. Although the news that PSA screening has led to overtreatment flitted in and out of the media, and the two investigations evaluated 258,693 men, it took THREE YEARS for the PSA test to be declared useless as a screening test for prostate cancer. I wonder how many unnecessary surgeries happened in the interim. (These findings may seem to contradict what I said above about metastasis, but they point to the fact that different types of cancer, and different subtypes, have different tendencies to metastasize. And many prostate cancers wouldn’t do so within a normal human lifespan.)
A final word: if you do everything right, and still get cancer, don’t feel guilty. Blame biology. For cancer is a consequence of being many-celled, of living longer, and of the inherent changeability of our DNA.