TMEN Programs

Program Area

Co-evolution of the Reactive Microenvironment in Prostate Cancer Progression
PI Name: ROWLEY, DAVID R Institute: BAYLOR COLLEGE OF MEDICINE Specific mechanisms of how the reactive microenvironment affects prostate cancer progression are unknown. Previous studies from our group have shown that the reactive microenvironment has properties and gene expression similar to wound repair biology. These include changes in stromal cell phenotype and altered neurogenesis. We have also shown that reactive stroma is tumor promoting. Carcinoma cells and nerves exhibit reciprocal interactions leading to elevated carcinoma proliferation and induced neurogenesis. The concurrent recruitment of myofibroblasts to premalignant PIN and carcinoma foci implicates a coordinated host response that promotes tumorigenesis. Importantly, our group has shown that specific biomarkers of this reactive microenvironment are predictive of recurrence of human prostate cancer. The integrated biology of this response and specific mechanisms are not yet understood at a level where more effective prognostics or novel therapeutics can be developed. Accordingly, the overall objectives of this project are to understand how reactive stroma and neurogenesis in the microenvironment function and interact mechanistically during the initiation and progression of early, organ confined disease. The endpoint of this study is to understand the key components, regulators, and mechanisms with a specific focus on early prostate cancer. We propose a Program composed of an Expression Analysis and Pathology Core and two interrelated Projects. Project 1 will address the co-evolution, origin, and specific regulators of reactive stroma cells. Project 2 will address the role of axonogenesis and neurogenesis in regulating early cancer. This study will provide fundamental data regarding the temporal and spatial composition, gene expression profiling, and potential regulators of the microenvironment in human tissues and mouse models. The overall goal is to provide novel pre-clinical data, from which more effective biomarkers and therapeutics can be developed that target the microenvironment of early prostate cancer.

Co-evolution of the Reactive Microenvironment in Prostate Cancer Progression

PI Name: ROWLEY, DAVID R
Institute: BAYLOR COLLEGE OF MEDICINE

Specific mechanisms of how the reactive microenvironment affects prostate cancer progression are unknown. Previous studies from our group have shown that the reactive microenvironment has properties and gene expression similar to wound repair biology. These include changes in stromal cell phenotype and altered neurogenesis. We have also shown that reactive stroma is tumor promoting. Carcinoma cells and nerves exhibit reciprocal interactions leading to elevated carcinoma proliferation and induced neurogenesis. The concurrent recruitment of myofibroblasts to premalignant PIN and carcinoma foci implicates a coordinated host response that promotes tumorigenesis. Importantly, our group has shown that specific biomarkers of this reactive microenvironment are predictive of recurrence of human prostate cancer. The integrated biology of this response and specific mechanisms are not yet understood at a level where more effective prognostics or novel therapeutics can be developed. Accordingly, the overall objectives of this project are to understand how reactive stroma and neurogenesis in the microenvironment function and interact mechanistically during the initiation and progression of early, organ confined disease. The endpoint of this study is to understand the key components, regulators, and mechanisms with a specific focus on early prostate cancer. We propose a Program composed of an Expression Analysis and Pathology Core and two interrelated Projects. Project 1 will address the co-evolution, origin, and specific regulators of reactive stroma cells. Project 2 will address the role of axonogenesis and neurogenesis in regulating early cancer. This study will provide fundamental data regarding the temporal and spatial composition, gene expression profiling, and potential regulators of the microenvironment in human tissues and mouse models. The overall goal is to provide novel pre-clinical data, from which more effective biomarkers and therapeutics can be developed that target the microenvironment of early prostate cancer.

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