​The Role of Mutant KRAS & p53 in Pancreatic Cancer Metastasis

Published by W Butcher on

By identifying a protein that disrupts the interplay between two key genetic drivers of pancreatic cancer, researchers from the University of Texas MD Anderson Cancer Center significantly dampened metastasis in preclinical studies with cell lines, genetic mouse models, and human pancreatic tumor tissue. According to results presented during the annual meeting of the American Association for Cancer Research (AACR), held April 10-15, the research team found that by targeting and inhibiting transcription factor CREB1 (cyclic AMP-responsive element binding protein1), they could decouple oncogenic KRAS from mutant tumor suppressor p53—driver genes mutated in most pancreatic cancer patients. “Through such decoupling of mutant KRAS and p53, we can start to ‘divide and conquer’ signaling pathways responsible for tumor maintenance and from those that promote metastasis,” said Michael Kim, MD, Assistant Professor in the Department of Surgical Oncology at MD Anderson.

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