NF1 loss of function as an alternative initiating event in pancreatic ductal adenocarcinoma
Gopalakrishnan Ramakrishnan, Parash Parajuli, Pura Singh, Creighton Friend, Eric Hurwitz, Céline Prunier, Mohammed S. Razzaque, Keli Xu, Azeddine Atfi
Abstract
-driven PDAC. Finally, we show an association between NF1 and p53 that is orchestrated by PML, and mosaic analysis with double markers demonstrates that concomitant inactivation of NF1 and Trp53 is sufficient to trigger full-blown PDAC. Together, these findings open up an exploratory framework for apprehending the mechanistic paradigms of PDAC with normal KRAS, for which no effective therapy is available.
Topics & Concepts
KRASPancreatic Intraepithelial NeoplasiaCancer researchHaploinsufficiencyPancreatic ductal adenocarcinomaBiologyMalignancyDuctal cellsDuctal carcinomaPancreatic cancerMedicineBreast cancerPancreasCancerMutationPhenotypeGeneticsGeneEndocrinologyPancreatic and Hepatic Oncology ResearchNeuroendocrine Tumor Research AdvancesNeuroblastoma Research and Treatments