Medical College of Wisconsin
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Stromal Inflammation in Pancreatic Cancer: Mechanisms and Translational Applications Pancreatic Cancer. 2nd Ed. Springer-Verlag New York DOI: 10.1007/978-1-4939-6631-8_55-1

Abstract

Pancreatic ductal adenocarcinoma is the most severe form of pancreatic cancer because of pronounced inflammation and desmoplasia leading to hypoxia, metabolic reprogramming, and immune suppression that ultimately promote tumor growth and metastasis. The conventional wisdom is that patient survival is hobbled by the inability of currently available therapies to penetrate the tumor and its dense stromal microenvironment. The pancreatic cancer stromal microenvironment is a heterogeneous population of cancer cells, immune cells, cancer-associated fibroblasts, vascular endothelial cells, and neurons. While a detailed understanding of the cells, mediators, and receptors influencing stromal dynamism continues to emerge, interactions between these cells influence tumor suppression as well as tumor promotion. The specific roles for the inflamed stroma in pancreatic cancer immune evasion, progression, metastasis, and therapeutic resistance likely depend on stage of tumor development and distinct biophysical features within the dynamic cellular micro-niches of the tumor. Uncovering the stromal mechanisms of tumor development and progression should prompt the discovery of key windows of opportunity for multimodal therapies in pancreatic cancer.

Author List

Boyle K, James MA, Tsai S, Evans DB, Dwinell MB.

Author

Michael James PhD Assistant Professor in the Surgery department at Medical College of Wisconsin


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