Gene alterations play a prominent role in driving cancer initiation and progression. Yet, mutations on oncogenes (those genes that promote tumorigenesis) only transform cells under certain cellular contexts. The mechanisms controlling neoplastic transformation (oncogenic competence) are poorly understood in pancreatic ductal adenocarcinoma (PDAC). We hypothesize that oncogenic competence relies on transcriptional programs and regulatory elements of pancreas development, which become activated during regeneration and can be exploited as novel theragnostic opportunities for this intractable disease. I will present the function of recently identified regulators of pancreas development that potentiate or prevent tumor initiation and the underlying molecular mechanism. Our overarching goal in the laboratory is to elucidate the interplay of gene alterations, transcriptional programs of development, and the tissue microenvironment in the initiation of PDAC.<\/p>\n
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