This Experimental Pathology Core is an integral component of the P01 for its expertise in characterizing the morphologic, molecular and metabolic phenotype of pancreatic cancer, from inception to metastasis, in their diverse states determined by targeted genetic manipulations and study of human tumor specimens. Genetic alterations, as evaluated in mouse models, will be translated and assessed in clinical PDAC tumors for validation purposes. This Core will work in close collaboration with the Project Investigators to achieve three specific aims: 1) to provide histology services and consultative expertise including centralized review in the pathologic evaluation of mouse and human pancreatic neoplasms;ii) to provide infrastructure and technical expertise for a variety of molecular pathologic assays;and iii) to evaluate and implement new ex vivo organotypic culture assays and advanced imaging and analysis technologies that will greatly facilitate these research goals in future.
These Aims encompass a wide variety of specialized techniques performed on genetically engineered mouse models, mouse xenograft models, and IRB-approved analysis of human patient tissue specimens. Services will be provided in close Integration with the BioBank Core, Imaging Core and GEM Core. Members of the Experimental Pathology Core have extensive experience in achieving both service-oriented goals as well as pioneering new molecular pathology research tools. The Core will seek to ensure a high quality of interpretive and developmental work to facilitate the goals of the P01.

Public Health Relevance

Pancreatic cancer is a disease without a cure. The pathologic evaluation of pancreatic cancer tissues under the microscope is crucial to understanding the how this disease starts, grows, and spreads to other parts of the body. The resources provided by the Experimental Pathology Core will provide investigators with crucial expertise in the analysis of human cancer tissue as well as tissues from mouse models of pancreatic cancer. Understanding of the cellular and molecular state of these cells upon genetic mutations and pharmacological treatments will provide crucial insight into molecular pathways that can be used to develop a cure for pancreatic cancer.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Research Program Projects (P01)
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Special Emphasis Panel (ZCA1-RPRB-0)
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University of Texas MD Anderson Cancer Center
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Biancur, Douglas E; Paulo, Joao A; Ma?achowska, Beata et al. (2017) Compensatory metabolic networks in pancreatic cancers upon perturbation of glutamine metabolism. Nat Commun 8:15965
Ravez, Séverine; Corbet, Cyril; Spillier, Quentin et al. (2017) ?-Ketothioamide Derivatives: A Promising Tool to Interrogate Phosphoglycerate Dehydrogenase (PHGDH). J Med Chem 60:1591-1597
Nejati, Reza; Goldstein, Jennifer B; Halperin, Daniel M et al. (2017) Prognostic Significance of Tumor-Infiltrating Lymphocytes in Patients With Pancreatic Ductal Adenocarcinoma Treated With Neoadjuvant Chemotherapy. Pancreas 46:1180-1187
Cancer Genome Atlas Research Network. Electronic address:; Cancer Genome Atlas Research Network (2017) Integrated Genomic Characterization of Pancreatic Ductal Adenocarcinoma. Cancer Cell 32:185-203.e13
Lu, Xin; Horner, James W; Paul, Erin et al. (2017) Effective combinatorial immunotherapy for castration-resistant prostate cancer. Nature 543:728-732
Lyssiotis, Costas A; Kimmelman, Alec C (2017) Metabolic Interactions in the Tumor Microenvironment. Trends Cell Biol 27:863-875
Pergolini, Ilaria; Morales-Oyarvide, Vicente; Mino-Kenudson, Mari et al. (2017) Tumor engraftment in patient-derived xenografts of pancreatic ductal adenocarcinoma is associated with adverse clinicopathological features and poor survival. PLoS One 12:e0182855
Sherman, Mara H; Yu, Ruth T; Tseng, Tiffany W et al. (2017) Stromal cues regulate the pancreatic cancer epigenome and metabolome. Proc Natl Acad Sci U S A 114:1129-1134
Shukla, Surendra K; Purohit, Vinee; Mehla, Kamiya et al. (2017) MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer. Cancer Cell 32:71-87.e7
Dey, Prasenjit; Baddour, Joelle; Muller, Florian et al. (2017) Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. Nature 542:119-123

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