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Updated: Mar 11, 2026

Mimicking and Manipulating Pancreatic Acinar-to-Ductal Metaplasia in 3-dimensional Cell Culture
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Oncogenic KRAS and the EGFR loop in pancreatic carcinogenesis-A connection to licensing nodes

Christian Schneeweis1, Matthias Wirth1, Dieter Saur1,2

  • 1a II. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität München , München , Germany.

Small Gtpases
|November 24, 2016
PubMed

Insights

Oncogenic KRAS drives pancreatic cancer via a novel EGFR signaling loop. This loop involves MYC and offers potential therapeutic targets for pancreatic ductal adenocarcinoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling

Background:

  • Epidermal growth factor receptor (EGFR) signaling is crucial for oncogenic KRAS-driven pancreatic ductal adenocarcinoma (PDAC).
  • The intricate signaling network of KRAS and its interaction with EGFR in PDAC remain poorly understood.
  • Understanding early signaling events is key to developing effective PDAC therapies.

Purpose of the Study:

  • To investigate early signaling events triggered by oncogenic KRAS in pancreatic epithelial cells.
  • To elucidate the role of EGFR signaling in KRAS-driven pancreatic tumorigenesis.
  • To identify potential therapeutic strategies for PDAC.

Main Methods:

  • Development of a novel murine primary pancreatic epithelial cell model.
  • Time-specific expression of mutant KrasG12D from its endogenous promoter.
  • Analysis of KrasG12D-induced signaling pathways and oncogene integration.

Main Results:

  • Identification of a KrasG12D-induced autocrine EGFR signaling loop in pancreatic cells.
  • Demonstration of MYC oncogene integration within this EGFR signaling loop.
  • Characterization of early molecular events in KRAS-driven pancreatic cancer.

Conclusions:

  • The KrasG12D-induced autocrine EGFR loop is a key driver in pancreatic cancer.
  • MYC integrates this loop, highlighting its significance in PDAC pathogenesis.
  • These findings suggest potential translational implications for targeting this pathway in PDAC treatment.
Keywords:
EGFRMYCautocrine signalingkraspancreatic cancer

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