Consequently, therapeutic targeting of Myc would be expected to have profound therapeutic utility, he says. In essence, we are trying to define the minimal mission critical targets that are needed to maintain a malignancy. Tumors acquire multiple mutations through their long histories, but not all are needed to maintain the cancer. In trying to design effective and smart therapies we cant afford to get bogged down in a history lesson about how the malignancy arose. We have to focus on what is sustaining the malignancy.
Our data show that many of the complex characteristics of tumors that are commonly thought to have arisen through the painstaking accumulation of many different mutations can arise directly as a consequence of c-Myc activation. Once this occurs you get unrelenting cell expansion, and all the other diverse characteristics of tumors seem to come along for the ride.
If the finding bears out with other oncogenes in animal models, and later in humans, the few interdependent mutations could prove key targets for therapy, he says.
The finding builds on previous research that Evan conducted in cell culture. (Cell 69 : 119-28, 3 April 1992). This earlier paper -- one of the 10 most cited papers in Molecular Biology and Genetics during the last decade -- indicated that oncoproteins such as c-Myc carr
Contact: Jennifer OBrien
415 476 2557
University of California - San Francisco