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Speeding discovery of the 'human cancer genome'

ly contribute to the cancerous cells' ability for unchecked proliferation or spread.

Simply sorting through those differences one by one takes time and money, said Lynda Chin of the Dana-Farber Cancer Institute and Harvard Medical School.

"There has to be a way to prioritize the effort," she said.

Chin's and Lowe's groups already relied on large-scale structural changes to chromosomes as a way of identifying areas of the genome with potential importance for cancer. Such chromosomal rearrangements often lead to the amplification of cancer-causing genes or the loss of genes that normally suppress tumor formation.

But as genome technology continues to improve, providing ever-increasing resolution, researchers have found more than they had expected, Chin said.

In human melanoma, for example, more than 100 genomic regions exhibit recurring structural changes, not all of which appear to be important, she said. One way to narrow down the number of regions is to look for chromosomal alterations found in both humans and in the complementary, or syntenic, regions of the mouse genome.

"If you are seeing the same event in different species, it becomes more likely that a common biological pressure is responsible--more likely that it is an important event," Chin said.

Using that strategy in the current study, Chin's group examined genetically engineered mice with melanoma that had developed an increased potential to spread, a process known as metastasis. Metastasis is a multistep process that requires and selects for tumor cells capable of escaping their normal microenvironment, traversing into and out of lymphatic or blood vessels, and proliferating in new "soil," the researchers said.

Metastasis is particularly important in skin cancer, Chin added, as the primary tumor is almost always curable. Once the cancer spreads from the skin to other parts of the body, however, it can
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Source:Cell Press


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