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NPRA signaling in the Tumor/Stroma Microenvironment Influences the Growth of Stem-like Cancer Cells
EP25407
Poster Title: NPRA signaling in the Tumor/Stroma Microenvironment Influences the Growth of Stem-like Cancer Cells
Submitted on 24 Feb 2017
Author(s): Ryan Green1 Mark C Howell1 Dr. Rajesh Nair1, PhD Shruti Padhee1, Ph.D Scott J Antonia, MD2 PhD Dr. Eva Samal1 Jit Banerjee1 Shyam Mohapatra1 Subhra Mohapatra1
Affiliations: 1University of South Florida 2Moffitt Cancer Center
This poster was presented at USF Health Research Day
Poster Views: 599
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Abstract: With growing evidence supporting the role of cancer stem cells (CSCs) in tumorigenesis, tumor heterogeneity, resistance to chemotherapeutic and radiation therapies, and the metastatic phenotype, the development of specific therapies that target CSCs holds promise for improving survival and quality of life for cancer patients, especially those with metastatic disease. Thus, there is an urgent need for the development of novel therapeutic agents that target lung CSCs, specifically agents that target CSC self-renewal, regeneration or differentiation processes. The natriuretic peptide receptor A (NPRA) signaling pathway is involved in tumor progression and may also be involved in CSC development. We reasoned that alterations to NPRA expression and signaling might lead to inhibition of CSC proliferation. To investigate this, we report the development of a tumor/stroma co-culture model to study and further define the role that NPRA plays in CSC development and drug resistance.
Summary: Therapies that target cancer stem cells hold promise for improving survival of cancer patients.There is an urgent need for the development of novel therapeutic agents that target lung CSCs. The natriuretic peptide receptor A signaling pathway is involved in tumor progression and CSC development. Changes to NPRA expression and signaling might lead to inhibition of CSC proliferation. We report a tumor/stroma co-culture model to study the role that NPRA plays in CSC development and drug resistanceReferences: 1Report abuse »
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