Beyond Kras: MYC Rules in Pancreatic Cancer
Author:
Publisher
Elsevier BV
Subject
Gastroenterology,Hepatology
Reference4 articles.
1. The basic helix-loop-helix transcription factor E47 reprograms human pancreatic cancer cells to a quiescent acinar state with reduced tumorigenic potential;Kim;Pancreas,2015
2. E47 governs the MYC-CDKN1B/p27KIP1–RB network to growth arrest PDA cells independent of CDKN2A/p16INK4A and wild-type p53;Scully;Cell Mol Gastroenterol Hepatol,2018
3. Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a;Serrano;Cell,1997
4. Deletion of Rb accelerates pancreatic carcinogenesis by oncogenic Kras and impairs senescence in premalignant lesions;Carrière;Gastroenterology,2011
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4. miR24–3p activity after delivery into pancreatic carcinoma cell lines exerts profound tumor-inhibitory effects through distinct pathways of apoptosis and autophagy induction;Cancer Letters;2021-04
5. Nanoformulation of BRD4-Degrading PROTAC: Improving Druggability To Target the ‘Undruggable’ MYC in Pancreatic Cancer;Trends in Pharmacological Sciences;2020-10
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