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Article

Metabolic reprogramming by mutant GNAS creates an actionable dependency in intraductal papillary mucinous neoplasms of the pancreas.

Gut - 10 Dec 2024

Makino Yuki, Rajapakshe Kimal I, Chellakkan Selvanesan Benson, Okumura Takashi, Date Kenjiro, Dutta Prasanta, Abou-Elkacem Lotfi, Sagara Akiko, Min Jimin, Sans Marta, Yee Nathaniel, Siemann Megan J, Enriquez Jose, Smith Paytience, Bhattacharya Pratip, Kim Michael, Dede Merve, Hart Traver, Maitra Anirban, Thege Fredrik Ivar

Abstract excerpt

BACKGROUND: Oncogenic 'hotspot' mutations of KRAS and GNAS are two major driver alterations in intraductal papillary mucinous neoplasms (IPMNs), which are bona fide precursors to pancreatic ductal adenocarcinoma. We previously reported that pancreas-specific Kras G12D and Gnas R201C co-expression in p48Cre; KrasLSL-G12D; Rosa26LSL-rtTA; Tg (TetO-GnasR201C) mice ('Kras;Gnas' mice) caused development of cystic...

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Share to Adenocarcinoma, Mucinous
Share to Carcinoma, Pancreatic Ductal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Line, Tumor

Share to Chromogranins

Share to Glycolysis

Share to GTP-Binding Protein alpha Subunits, Gs

Share to Pancreatic Neoplasms

Share to Proto-Oncogene Proteins p21(ras)

Source

Identifiers

PMID: 39277181
DOI: 10.1136/gutjnl-2024-332412

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Metabolic reprogramming by mutant GNAS creates an actionable dependency in intraductal papillary mucinous neoplasms of the pancreas.PMID 39277181Read ↗

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