Cancer Gene Markers As researchers have learned more about what causes a cell to become cancerous, they have begun to realize that treatments that work for some tumors involving gene mutations are useless for others. Identifying whether breast cancer patients may have mutations in such genes could help doctors tailor the most effective treatment for individual patients. One study conducted by researchers at Duke University’s Comprehensive Cancer Center identified a liver cancer gene that is also defective in more aggressive breast tumors that may not respond to certain common types of chemotherapy. “People tend to think of breast cancer as a single disease,” warns Randy Jirtle, professor of radiation oncology, “but in reality there are many independent events in the cell that can lead to uncontrolled growth. We are beginning to learn that one size doesn’t fit all in cancer treatment.” To help sort out the roles of different genes in tumor growth, the researchers studied the role of a gene called mannose 6-phosphate/insulin-like growth factor II receptor (M6P/IGF2r), which normally helps control cell growth and suppress tumor formation. In previous studies of liver cancer, researchers demonstrated that M6P/IGF2r is often mutated in early stage tumors, demonstrating the important role it plays in the initial progression of this type of cancer. To determine if the gene also plays a role in breast cancer, the researchers studied tissue from breast tumors of 62 patients. Normally, people have two copies of the gene. If one copy of the gene mutates, the good copy can compensate. But when the good copy is deleted through a second mutation, the tumor-fighting ability is lost completely. In 30 percent of the breast cancers studied, the tumor-fighting gene was lost. Doctors commonly use two broad classes of chemotherapy to treat cancer; cytotoxic agents, which kill all actively growing cells in the body, and cytostatic agents, which induce tumor cells to self-destruct. The commonly used cytostatic drug tamoxifen appears to work, in part, by prompting cells to produce larger quantities of TGFb1, a potent tumor growth inhibitor when present in high levels. To become activated, TGFb1 requires the M6P/IGF2 receptor. If the receptor is missing or inactive because of mutation, TGFb1 can’t do it’s job. “Many times it is difficult to discern which patients will respond to tamoxifen treatment,” Jirtle said. “This study provides a first step in what we believe will be the future of breast cancer treatment; customizing therapy to each individual case.”
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