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Loss of the TGF-β antiproliferative response is a hallmark in human cancers.Tumor cells have developed a number of strategies to escape from TGF-β control.One major mechanism to resist the cytostatic effect of TGF-β is through inactivating mutations/deletions in the TGF-β signaling pathway, which frequently occur in gastrointestinal and pancreatic cancer.For example, tumor suppressor Smad4/DPC4-the central transducer of TGF-β signaling-is deleted in more than half of pancreatic cancer patients.However, not all types of cancers harbor deletion or mutations in the Smad4 gene.We have taken various approaches to study how TGF-β tumor suppressor function is regulated in normal and cancer cells.We found that activation of many oncoproteins can cause TGF-β resistance.Our studies provide invaluable information on the oncoprotein-tumor suppressor interplay in tumorigenesis.