Synthesis a Publication of UC Davis Cancer Center

Beyond conventional treatments
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Researchers know that cancerous cells often have lower concentrations of oxygen than healthy ones. In normal situations oxygen-poor cells would die naturally. But genetic mutations, some of them possibly involving a tumor supressor gene known as p53, allow oxygen-poor cells to proliferate and to become resistant to radiation and chemotherapy, which depend on chemical reactions involving oxygen to be effective.

Poorly oxygenated cells also reproduce more slowly, which helps them thrive underneath the radar of chemotherapy drugs that attack rapidly-multiplying cells.

Hypoxic cytotoxins reverse this effect by releasing oxygen free radicals into cancers cells, causing the cells to self-destruct. Happily, this same process also makes cancer cells more responsive to conventional treatments, and with fewer side effects.

"A large, randomized trial in Europe using a drug called tirapazamine doubled the survival of patients with metastatic lung cancer," Gandara notes. "That's quite dramatic." Phase 2 trials of tirapazamine in lung cancer will begin at UC Davis this year.

Another novel approach to cancer therapy involves Herceptin, the trade name for the drug trastuzumab. Herceptin is a monoclonal antibody, a mass-produced human protein that binds to specific cancer cells with a lock-and-key type of mechanism. Some monoclonal antibodies are loaded with chemotherapy drugs or radiation, allowing oncologists to give a targeted dose of cancer-killing drugs to a specific site. Other monoclonal antibodies, Herceptin included, block growth factor proteins responsible for cancer proliferation.