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New view of tumors' evolution
Date:3/13/2014

studied a strain of mice that lacks two key tumor-suppressor genes, p53 and Rb. These mice develop small cell lung cancer, but scientists don't know exactly how the cancer progresses or which subsequent genetic alterations drive tumor growth.

In studies of human small cell lung cancer, it has been difficult to identify these driver mutations because potent carcinogens in cigarette smoke produce many mutations, most of which don't affect tumor growth. In the mouse model of the disease, fewer mutations arise because the mice are not exposed to cigarette smoke, making it easier to identify the key drivers.

Mice lacking p53 and Rb, the two most commonly mutated tumor suppressors in human small cell lung cancer, develop lung tumors that closely mimic the progression of human small cell lung cancer. These tumors are highly metastatic and usually spread to the lymph nodes near the lungs and then to the liver. The researchers isolated DNA from these tumors and analyzed the genetic alterations that occurred, including genetic mutations as well as changes in the number of copies of a gene or chromosome.

First, the researchers compared genetic alterations that appeared early and late in cancer development. They found that early on, tumors accumulate many extra copies of a gene called Mycl1, a known oncogene that helps cells ignore signals to stop growing. Because Mycl1 is mutated so early, it is found in nearly all of the tumor cells, making it a good drug target, McFadden says. There are currently no cancer treatments that specifically target Mycl1, but scientists are now working on drugs that target a closely related oncogene, MYC.

Later in tumor progression, the mouse cancer cells lose a gene called Pten, which has previously been found mutated in about 20 percent of small cell lung cancer patients. In normal cells, Pten regulates a critical signaling pathway called PI3K, which influences many aspects of cell growth and survival. When Pt
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Contact: Sarah McDonnell
s_mcd@mit.edu
617-253-8923
Massachusetts Institute of Technology
Source:Eurekalert

Page: 1 2 3

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