Document Type

Abstract

Publication Date

2-11-2026

Academic Year

2025-2026

Comments

Presented at the 2026 Scholarly Inquiry (SI) Research Project Symposium.

Abstract

Introduction
Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer-related mortality worldwide. While the only curative treatment for PDAC is surgical excision of the tumor, often surgery is ineffective due to early metastasis to other organs. A better understanding of PDAC’s risk factors would contribute to earlier PDAC diagnoses and thus more effective surgical resections before metastasis occurs.

One pathology related to PDAC is metabolic dysfunction-associated steatotic liver disease (MASLD), a metabolic disease leading to triglyceride accumulation in the liver. MASLD is known to cause worse PDAC outcomes versus non-MASLD PDAC. Further elucidating the mechanism through which MASLD increases PDAC’s severity would therefore contribute to earlier PDAC diagnoses and treatment. As such, the present research specifically identifies gene signatures that distinguish MASLD- from non-MASLD-related pathology in PDAC patient samples.

Methods
Patients with PDAC (N=149) were first ascribed diagnoses of MASLD or non-MASLD based on clinical chart data and published clinical algorithms. Next, pancreatic tumor samples from these patients were sequenced via whole transcriptome sequencing and analyzed for differential gene expression between the MASLD and non-MASLD groups.

Results
36 genes were identified as differentially expressed between MASLD and non-MASLD in PDAC patients (false discovery rate < 0.05).

Conclusions
The identified genes represent further understanding of the contributing factors to PDAC’s severity, enabling earlier diagnosis and treatment of PDAC. Future steps include using spatial transcriptomics to determine how exactly MASLD influences the tumor microenvironment of PDAC and building custom sequencing analysis algorithms to allow for more sensitive gene signature detection.

Language

English

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