Pink ribbons are for breast cancer, dark blue ribbons are for colon cancer, white ribbons are for lung cancer, gray ribbons are for brain cancer, emerald green ribbons are for liver cancer, and zebra-striped ribbons are for carcinoid cancers. January is cervical cancer awareness month, represented by the teal-and-white ribbon. February is for gallbladder and bile duct cancers, with a kelly green ribbon to represent them. And so on.
As cancer kills more people than ever before, it is natural for us to seek affiliation with those affected by a similar cancer type. Breast cancer patients, survivors and their friends and relatives coalesce their efforts to create awareness and raise funds for breast cancer research and prevention. The same goes for those affected by other cancers, and there is nothing wrong with that. At a time when the National Cancer Institute is losing purchasing power at a scary pace, and when cancer researchers struggle to fund their laboratories, every fundraising and educational effort from organized citizens makes a big difference.
However, we must be very cautious about how brightly we color our ribbons.
If there is a key lesson that we have learned over the last 40 years of research, it is that cancer is more a disease of genes than a disease of specific tissues. We know for a fact that mutations in oncogenes and tumor suppressor genes drive cancer. Most importantly, we have learned that many of these genes are commonly mutated across cancers of different tissue origin. Mutations in the RAS oncogene are commonly found in many cancer types. The same is true for mutations in the tumor suppressor gene p53. A pancreatic cancer patient and a lung cancer patient whose tumors harbor mutations in RAS and p53 have much more in common than they might think. Targeted therapies aimed at restoring the normal activities of RAS and p53 may help both of them.
On the other hand, two women with breast cancer may be suffering from drastically different diseases, due to the distinct genetic alterations found in their tumors. A "triple negative" breast cancer patient carries a tumor that does not express the estrogen receptor, the progesterone receptor or the growth factor receptor known as HER2. Her prognosis and course of treatment are radically different from her friend with "triple positive" breast cancer. The "triple negative" patient will not benefit from drugs that oppose estrogen action or that block the HER2 oncoprotein. Her prognosis is worse than that of her "triple positive" friend, who would benefit from these drugs.
Therefore, the specialization of our research and educational efforts based solely on a given cancer's tissue of origin could have detrimental aspects. We should prevent the segregation of researchers and educators along the wrong boundaries. As the age of personalized molecular medicine advances, we should recognize the molecular commonalities across diverse cancer types and act accordingly. Some cancer funding agencies put too much emphasis during their grant review process on whether the applicant scientist has specialized expertise on this or that tissue, ignoring that said scientist may be an expert on a given oncogene or tumor suppressor gene relevant to many cancer types. A mechanistic discovery made by this scientist while employing pancreatic cancer cells in his experiments may greatly impact on the diagnosis and treatment of lung cancer patients whose tumors harbor similar genetic alterations. To discourage his research efforts because he has not focused on a single tissue of origin will be a great disservice. We must think more about genes, less about specific tissues.
I look forward to the day when our fundraising, funding and educational efforts fully recognize the genetic basis of our cancers. Maybe one day in the near future we will have purple ribbons for RAS, dark blue ribbons for p53 and pink ribbons for HER2.
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