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Digital Publisher
Digital Commons at St. Mary's University
Publication Date
Spring 2025
Keywords
Pancreatic ductal adenocarcinoma (PDAC) ; pancreatic cancer; genetic mutation
Description
Pancreatic ductal adenocarcinoma (PDAC) is an exocrine pancreatic cancer. It is one of the most lethal types of cancer and is projected to become the second leading cause of cancer-related deaths by 20401 . One major challenge in treating PDAC is drug resistance and the lack of effective treatments. Oncogenic KRAS mutation and loss of function mutation in tumor suppressor genes including P16, TP53, and SMAD4 are found in most PDAC patients. It is unclear whether the different driver mutations can affect the tumor responses to chemo- and targeted therapy. Gemcitabine, a chemotherapy drug, is a cytotoxic agent that has been used for treating pancreatic cancer2 . RMC7977, a most recently developed drug that targets active RAS proteins, shows strong tumor-specific effects in pre-clinical models of PDAC3 . Transcription factors are proteins that regulate gene expression, which may play a role in cancer drug resistance. We proposed to perform an overexpression screen using a commercially available cDNA library of transcription factors in our primary human pancreatic acinar organoids, aiming at identifying key transcription factors that contribute to drug resistance.
The research project aims to characterize the drug response from PDAC cells harboring different genetic mutation backgrounds. This will provide important guidance for precision medicine and pharmacotyping for individual PDAC patients to predict their drug response phenotypes and characteristics resulting from various genetic backgrounds.
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1 page
City
San Antonio, Texas
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.
