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Oncogenic GNAS Uses PKA-Dependent and Independent Mechanisms to Induce Cell Proliferation in Human Pancreatic Ductal and Acinar Organoids
Journal article   Open access   Peer reviewed

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

Ridhdhi Desai, Ling Huang, Raul S Gonzalez and Senthil K Muthuswamy
Molecular cancer research, v 22(5), pp 440-451
02 May 2024
DOI: https://doi.org/10.1158/1541-7786.MCR-23-0199
PMID: 38319286
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9928035View
Published, Version of Record (VoR)Open Access (License Unspecified),  Open

Abstract

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

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13 Record Views
7 citations in Web of Science
7 citations in Scopus

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UN Sustainable Development Goals (SDGs)

This publication has contributed to the advancement of the following goals:

#3 Good Health and Well-Being

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Collaboration types
Domestic collaboration
Web of Science research areas
Cell Biology
Oncology
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