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Related Experiment Videos

Re-engineering the Pancreas Tumor Microenvironment: A "Regenerative Program" Hacked.

Gerard I Evan1, Nasun Hah2, Trevor D Littlewood3

  • 1Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom. evans@salk.edu gie20@cam.ac.uk.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|April 5, 2017
PubMed
Summary

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Pancreatic ductal adenocarcinoma (PDAC) exploits the pancreas's regenerative repair programs through super enhancers. Targeting these super enhancer networks offers a promising therapeutic strategy for pancreatic cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) is characterized by proliferative, invasive tumor cells and a dense desmoplastic stroma.
  • The tumor microenvironment in PDAC is inflammatory and immunosuppressive, crucial for disease progression.
  • PDAC's unique phenotype arises from oncogenes hijacking the pancreas's regenerative repair programs, regulated by super enhancer networks.

Purpose of the Study:

  • To explore the role of super enhancers in pancreatic cancer development and maintenance.
  • To identify super enhancer networks as a potential therapeutic vulnerability in PDAC.
  • To discuss novel therapeutic strategies targeting epigenetic regulators of super enhancer-dependent transcription.

Main Methods:

  • Review of existing literature on PDAC hallmarks and the role of super enhancers.

Related Experiment Videos

  • Analysis of the interdependence between oncogenically activated pancreatic epithelium and its stroma.
  • Discussion of drugs targeting epigenetic modifiers (e.g., HDACs, DNMTs, BET proteins).

    • Main Results:

    • Super enhancers are critical for cell identity and maintenance, playing a pivotal role in the pancreas-specific tumor phenotype.
    • Disrupting super enhancer-driven repair networks could disproportionately affect tumor cells compared to normal pancreatic tissue.
    • Epigenetic drugs targeting super enhancer-dependent transcription have shown feasibility in treating various cancers, including PDAC.

    Conclusions:

    • Pancreatic adenocarcinomas rely on super enhancer transcriptional mechanisms, presenting a targetable vulnerability.
    • Targeting these super enhancer networks offers a novel therapeutic avenue for intractable pancreatic cancer.
    • Interfering with epigenetic regulators provides a feasible strategy for disrupting PDAC's reliance on super enhancers.