GPCR Signaling in PDA: Calcium, cAMP, and Ras Activation in Pancreatic Ductal Adenocarcinoma
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: 15 February 2026 | Viewed by 18
Special Issue Editor
Special Issue Information
Dear Colleagues,
G protein-coupled receptor (GPCR) signaling promotes the initiation, progression, and metastasis of pancreatic ductal adenocarcinoma (PDA). For this Special Issue on GPCR pathways in PDA, we welcome research manuscripts and reviews of clinical studies and cutting-edge basic research using PDA model systems. GPCR pathways are integral to pancreatic diseases associated with a high risk of progression to PDA, including chronic pancreatitis and late-onset diabetes. Second messengers generated by GPCR activation, such as cAMP and intracellular calcium, provoke the formation of intraductal papillary mucinous neoplasm (IPMN) and pancreatic intraepithelial neoplasia (PanIN), precancerous lesions associated with initiation and progression to PDA. GPCRs engage in cross talk with receptor tyrosine kinases (RTKs) in the activation of oncogenic Kras isoforms that are found in 90% of human PDA patients. GPCRs promote cancer proliferation and regulate cancer–stromal interaction and epithelial-to-mesenchymal transition (EMT), leading to metastasis. Epigenetic alterations associated with progression in Kras-dependent PDA interact with the GPCR, Wnt, and Hedgehog pathways. GPCRs are the largest protein family of drug targets, thereby offering untapped potential for therapeutic intervention. We invite manuscripts exploring novel insights into the mechanisms behind tumor growth, signaling in the microenvironment, immune interactions, diagnosis, and treatment options related to GPCR signaling.
Dr. Thomas Wilkie
Guest Editor
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Keywords
- G protein-coupled receptor (GPCR)
- receptor tyrosine kinases (RTK)
- oncogenic Kras
- pancreatic ductal adenocarcinoma (PDA)
- epigenetic regulation
- Wnt and Hedgehog (HH)
- second messengers (cAMP and intracellular calcium)
- acinar to ductal metaplasia (ADM)
- tumor microenvironment
- therapeutic drugs list of solicited contributors
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