It won't be easy to find and take aim at stem cells, since they're apt to look different from patient to patient, says Craig Jordan, a molecular biologist at the University of Rochester Medical Center whose lab is one of several working to develop new cancer stem cell treatments. But some drugs may already be blasting these cells. Gleevec may work so well because it eliminates leukemia stem cells, for example. And the breast cancer drug Tykerb appears to cut the number of breast cancer stem cells.
As well as explaining how a tumor recurs, some experts theorize that stem cells may offer clues to a cancer cell's deadliest function: metastasis. Perhaps the stem cells themselves stealthily leave the site of the original tumor and lodge elsewhere, sometimes hiding for years before beginning to grow again. Or perhaps they are capable of producing those highly mobile cells.
Understanding how cancer operates in the body requires looking beyond the cancer cell itself, at the tiny neighborhood of normal cells that surround it. Cancer that wants to grow and thrive has to recruit nearby cells to its cause, just as someone might borrow a cup of sugar from a neighbor. For example, the cascade of chemicals involved in the body's inflammatory response may help the cell invade healthy tissue, says David Cheresh, vice chair of pathology at Moores Cancer Center at the University of California-San Diego. And the various healthy surrounding tissues and cells play their part, too. One class of drugs, including Avastin for advanced colon, lung, and breast cancer, already buys some patients extra time by targeting one part of the tumor's outreach to its neighborhood: its recruitment of blood vessels to fuel its growth.
A friendly microenvironment is also key to metastasis. Ties between a cancer cell and its neighbors are already strong by the time a primary tumor grows, says Lynn Matrisian, chair of cancer biology at Vanderbilt University. But when a cancer cell travels to a distant organ, "in my mind, there's an opportunity to intervene" before neighborly relationships are cemented, says Matrisian. Indeed, drugs used to prevent osteoporosis can also make the bone less hospitable to metastatic cells from breast, prostate, and other cancers.
Metastasis might also be foiled by immunotherapy, which prompts the body's own defenses—usually muted or silenced by cancer—into action. At the Fred Hutchinson Cancer Research Center in Seattle, researchers reported in June that an experimental treatment involving the cloning of a patient's immune cells (and injection of a superdose) apparently sent one metastatic melanoma patient into remission. The treatment didn't have the same effect on several other patients. Johns Hopkins researchers are working on therapeutic vaccines against pancreatic and breast cancers.
Seeking the Earliest Signs
Of course, metastasis and the deaths that it causes could be avoided much more handily if more cancers were easily detectable early on, as are breast, colorectal, and a small handful of other cancers. "The [number of] cancer survivors is going up because we are catching things early, before they can spread," says geneticist George Miklos, whose Sydney-based consultancy advises companies on genetics and molecular medicine.
Jane Tervooren, now 55, believes early detection saved her life. She felt for years that she was destined to get cancer; her grandmother died of ovarian cancer, and her mother did too, after surviving breast cancer. "My mother made me swear, on her deathbed, that I'd get my ovaries removed," she remembers. She did that and registered with the Family Risk Assessment Program at the Fox Chase Cancer Center in Philadelphia, where she eventually discovered she carried an inherited mutation in a gene, BRCA1, associated with ovarian and breast cancer. Because of her heightened risk, she received preventive medication that blocks estrogen production and had her breasts monitored frequently. Earlier this year, a mammogram detected very early-stage cancer, and after surgery, she's being treated with chemo.