Senescence in pancreatic carcinogenesis: From signalling to chromatin remodelling and epigenetics

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Abstract

Mutational activation of K-Ras is a key genetic event involved in the initiation of pancreatic carcinogenesis. However, K-Ras generally fails to transform precursor lesions into invasive cancers due to activation of powerful fail-safe programmes that counteract transformation and growth. The importance of cellular senescence, a permanent cell growth arrest, is increasingly being recognised as a critical fail-safe programme in pancreatic carcinogenesis. Emerging evidence suggests that oncogene-induced senescence requires transcriptional induction of the CDKN2A gene locus as well as comprehensive chromatin modifications involved in epigenetic silencing of pro-proliferative genes. Moreover, recent work in pancreatic cancer mouse models proposes that inactivation of the CDKN2A tumour suppressor locus is the molecular switch required for senescence evasion and unleashed K-Ras driven malignant transformation in the pancreas.

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Singh, S. K., & Ellenrieder, V. (2013). Senescence in pancreatic carcinogenesis: From signalling to chromatin remodelling and epigenetics. Gut, 62(9), 1364–1372. https://doi.org/10.1136/gutjnl-2012-302793

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