udy, the scientists used gene knockouts to create mice whose cells lacked crucial molecules whose role is to guard the genome from instability and chaos in the DNA. As a result, the mice developed T-cell acute lymphoblastic leukemia/lymphoma, or T-ALL, and the cancer cells exhibited "rampant genome instability" leading to a complex pattern of mutations, chromosomal rearrangements, gene amplifications and gene deletions similar to those in human solid tumors.

The mouse model's close resemblance to human T-ALL enabled the scientists to rapidly and efficiently identify two genes, FBXW7 and PTEN, to be commonly deleted or mutated in this type of human cancer.

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Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
24-May-2007

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