TCGA’s research has revealed some overlap in mutations causing different cancers. For example, the BRAF mutation, prominent in melanoma, also -figures—albeit less strongly—in colon and other cancers. And Gleevec, which targets a gene common to everyone who suffers from CML, is now used to treat several other rare cancers. Because of the success of genetic targeting, some authorities have come to believe that the primary cancer site may not ultimately be the primary focus of treatment. That is, rather than treating colon cancer, oncologists may treat, say, the BRAF mutation, regardless of its location.
The newest frontier: slowing cancer’s spread
Oncologists point out that patients usually don’t die from the original cancer. Nearly 90 percent of cancer deaths are due to metastasis, which is the migration of tumor cells from the primary site to other parts of the body. So the story of cancer is often a tale of traveling cells that, if they grow, destroy the function of distant organs. In other words, if doctors can figure out how to slow or halt the spread, they will probably save lives.
Metastasis is driven by genes, which direct where a cancer will spread, explains Joan Massagué, PhD, chair of the Cancer Biology and Genetics Program at MSKCC. Tissues in different parts of the body have barriers against foreign invaders, so the cancerous cells that succeed must have the propensity to bypass one or another of these obstacles, such as the normally impenetrable network of capillaries in the lungs and the brain. Researchers at MSKCC have found particular genes that enable cancer cells to multiply, as well as other genes that do the opposite and are missing in cancer tumors that have spread.
Says Larry Norton, MD, deputy physician-in-chief for Breast Cancer Programs at MSKCC: “With breast cancer, we have evidence that the primary cancer sends out little packets of information called exosomes that go to organs, particularly the lung, and start the process of tumor formation even before the cancer cells get there. Whenever you have a chemical signal and a receiver for the signal, you have the potential for intervention. And
this is part of what targeted therapy is all about.”
The last question I asked all the cancer researchers I spoke to was, “Suppose I were to go on vacation. How long would I have to go away to come back and find the whole landscape changed?” Those who were willing to answer gave a variety of responses. “At the pace we are going in melanoma, a five-year vacation would make a big difference,” said UCLA’s Antoni Ribas. MSKCC’s Larry Norton replied, “It’s changing all the time. Your vacation should be a weekend. In 10 years, I hope, I am going to have to find another job.”
Most cancer researchers, I think, would agree with Brian Druker of Oregon Health and Science University, who observed, “If you looked at World War II prior to D-Day, you’d have said, ‘We’re never going to crack this.’ My view is that at least we’ve arrived on the beaches.”
Katharine Davis Fishman’s last article for Morewas the award-winning “Boning Up on Bone Drugs,” June 2010.
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