Literature DB >> 26315515

The Triple-Code Model for Pancreatic Cancer: Cross Talk Among Genetics, Epigenetics, and Nuclear Structure.

Gwen A Lomberk1, Raul Urrutia2.   

Abstract

Pancreatic adenocarcinoma is painful, generally incurable, and frequently lethal. The current progression model indicates that this cancer evolves by mutations and deletions in key oncogenes and tumor suppressor genes. This article describes an updated, more comprehensive model that includes concepts from the fields of epigenetics and nuclear architecture. Widespread use of next-generation sequencing for identifying genetic and epigenetic changes genome-wide will help identify and validate more and better markers for this disease. Epigenetic alterations are amenable to pharmacologic manipulations, thus this new integrated paradigm will contribute to advance this field from a mechanistic and translational point of view.
Copyright © 2015 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Epigenetics; Pancreatic adenocarcinoma; Triple-code hypothesis

Mesh:

Substances:

Year:  2015        PMID: 26315515      PMCID: PMC4556141          DOI: 10.1016/j.suc.2015.05.011

Source DB:  PubMed          Journal:  Surg Clin North Am        ISSN: 0039-6109            Impact factor:   2.741


  116 in total

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6.  Epigenomics of Pancreatic Cancer: A Critical Role for Epigenome-Wide Studies.

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7.  HDAC inhibitors, MS-275 and salermide, potentiates the anticancer effect of EF24 in human pancreatic cancer cells.

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10.  Nuclear Envelope Regulation of Oncogenic Processes: Roles in Pancreatic Cancer.

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