( ug regimen prolongs survival. Whil...)Speeding discovery of the 'human cancer genome'

While a handful of genes have been linked to liver cancer, "how specific lesions interact to produce its aggressive characteristics remains poorly understood."

Lowe's team relied on mice with specific pathological changes known to play a role in some liver cancers. They then searched for other spontaneous mutations in the animals' tumors and compared them to recurrent alterations observed in the human disease.

That comparison narrowed the field to two genes that appear to "drive" liver tumors in both species: a gene called cIAP1, known to inhibit cell death, and a transcription factor called Yap. Both are required to sustain rapid growth of the tumors, they showed.

As the chromosomal region under study is found in five to ten percent of human tumor types, including lung, ovarian, esophageal, and liver carcinomas, the findings suggest the overall contribution of cIAP1 and Yap to human cancer may be substantial, the researchers said.

Their new mouse model now offers an "excellent setting" for preclinical tests of the potential of cIAP1 and Yap as targets for new cancer therapies, they added.

Taken together, the papers demonstrate a general principle with real importance for cancer patients, Chin said.

"Robust, stringent and biologically relevant systems for filtering, annotating, and prioritizing the efforts of cancer geneticists and biologists will be essential to facilitate and accelerate the translation of our genomic knowledge into cancer drugs that will impact patient survival," she wrote.