- What prompts certain cells to become cancerous and grow into tumors? For a while researchers figured the answer lay entirely in the way key genes became damaged, or mutated, over time.
- Over the past decade, however, investigators have uncovered many other contributing factors—from bacteria living in the intestine to epigenetic switches that turn various genes on and off.
- Unraveling this growing complexity makes understanding cancer harder than ever, but it also offers unexpected avenues to explore for the development of new treatments.
More In This Article
Things are rarely as simple as they seem, and what appears to be complex may be no more than ripples on the surface of a fathomless ocean. The mechanics of malignancy—a single cell acquiring mutation upon mutation until it spirals down the rabbit hole of cancer—was neatly described by two scientists, Douglas Hanahan and Robert A. Weinberg, in a sweeping synthesis published in 2000 called “The Hallmarks of Cancer.”
The idea of cancer occurring as an accumulation of mutations to a normal cell goes back decades. But it was Hanahan and Weinberg who assimilated a growing mass of laboratory results and theoretical insights into six characteristics that a cancer cell must acquire as it develops into the would-be creature called a tumor. It must acquire the ability to stimulate its own growth and to ignore signals admonishing it to slow down (that is where oncogenes and tumor suppressors come in). It must learn to circumvent the fail-safe mechanisms that cause even slightly disabled cells to destroy themselves and to defeat the internal counters—the telomeres found on the ends of chromosomes—that normally limit the number of times a cell is allowed to divide. It must learn to initiate angiogenesis—the sprouting of its own blood vessels—and finally to eat into surrounding tissue and to metastasize.
This article was originally published with the title The Long Trail of Cancer's Clues.