Oncogenic GNAS Uses PKA-Dependent and Independent Mechanisms to Induce Cell Proliferation in Human Pancreatic Ductal and Acinar Organoids

Mol Cancer Res. 2024 May 2;22(5):440-451. doi: 10.1158/1541-7786.MCR-23-0199.

Abstract

The study identifies an opportunity to discover a PKA-independent pathway downstream of oncogene GNAS for managing IPMN lesions and their progression to PDAC.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acinar Cells / metabolism
  • Acinar Cells / pathology
  • Carcinoma, Pancreatic Ductal / genetics
  • Carcinoma, Pancreatic Ductal / metabolism
  • Carcinoma, Pancreatic Ductal / pathology
  • Cell Proliferation*
  • Chromogranins* / genetics
  • Chromogranins* / metabolism
  • Cyclic AMP-Dependent Protein Kinases* / genetics
  • Cyclic AMP-Dependent Protein Kinases* / metabolism
  • GTP-Binding Protein alpha Subunits, Gs* / genetics
  • GTP-Binding Protein alpha Subunits, Gs* / metabolism
  • Humans
  • Organoids* / metabolism
  • Organoids* / pathology
  • Pancreatic Ducts / cytology
  • Pancreatic Ducts / metabolism
  • Pancreatic Ducts / pathology
  • Pancreatic Neoplasms* / genetics
  • Pancreatic Neoplasms* / metabolism
  • Pancreatic Neoplasms* / pathology

Substances

  • GNAS protein, human
  • GTP-Binding Protein alpha Subunits, Gs
  • Chromogranins
  • Cyclic AMP-Dependent Protein Kinases