ArticleStem cell research & therapy2026
Obesity and diabetes associated with dysregulation of mevalonate pathway markers and progression from pancreatic intraepithelial neoplasia to invasive pancreatic tumor.
Article in Stem cell research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCholesterol metabolic reprogramming plays a key role in pancreatic cancer progression by regulating the tumor immune microenvironment (TIME) and influencing responses to immunotherapy. Pancreatic intraepithelial neoplasia (PanIN) is the most common precursor lesion of pancreatic ductal adenocarcinoma (PDAC), a malignancy that commonly occurs in individuals with high BMI and type 2 diabetes mellitus (T2DM). Key metabolic markers (SOAT1 and SREBP2), the tumor suppressor P53, and the immune marker CD8 are implicated in PanIN initiation, PDAC progression, and subsequent metastasis, but their associations-particularly for those that are potentially targetable-remain poorly defined.
methodsUsing publicly available PDAC datasets from the GEO database, we conducted in silico analyses to investigate the genes of interest. Additionally, we used laser capture microdissection to isolate specific cells from pancreatic cancer tissues obtained from patients. We performed translational research using 17 tumor samples, as well as 17 microdissected PanIN lesions and matched normal tissues. Protein expression analysis was further conducted on a larger cohort, including 65 PanIN lesions and 157 tumor tissues from PDAC patients.
resultsOur data identify a dual-direction expression pattern in obese and diabetic patients, with elevated levels of SOAT1, SREBP2, and P53, and reduced CD8 expression, suggesting a coordinated metabolic and immunological alteration in pancreatic cancer. High BMI and T2DM, recognized as independent risk factors for PDAC, are significantly associated with dysregulation of key markers involved in the mevalonate pathway and the TIME, potentially contributing to PanIN and PDAC progression.
conclusionThese findings warrant further longitudinal and mechanistic studies to clarify whether metabolic modulation may influence PDAC risk or clinical outcomes.
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