A new, effective and high-yield approach for identifying liver tumor suppressors
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* Corresponding author: Lewis R Roberts roberts.lewis@mayo.edu
1 Department of Internal Medicine, McLaren Regional Medical Center, 401 S Ballenger Highway, Flint, Michigan 48532, USA
2 Miles and Shirley Fiterman Center for Digestive Diseases, College of Medicine, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905, USA
Genome Medicine 2009, 1:26 doi:10.1186/gm26
Published: 26 February 2009Abstract
Despite recent advances in research in hepatocarcinogenesis, we still lack a comprehensive view of the major pathways involved in liver carcinogenesis. Current concepts suggest that a limited number of molecular alterations involving oncogene activation and tumor suppressor inhibition are responsible for initiation of cancer. A recent publication by Zender et al. utilizes a combination of high-resolution comparative genomic hybridization, short hairpin RNA inhibition of target genes at the locations of focal genomic deletions, and a primed cell mosaic mouse model to identify novel tumor suppressors in hepatocellular carcinoma. This exciting new model promises to provide additional insights into the mechanisms of carcinogenesis.