Effect of genetic background on the initiation and progression of mouse prostate cancer driven by MYC overexpression and Pten loss
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Date
2020-01-01
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Department
Biological Sciences
Program
Biological Sciences
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This item may be protected under Title 17 of the U.S. Copyright Law. It is made available by UMBC for non-commercial research and education. For permission to publish or reproduce, please see http://aok.lib.umbc.edu/specoll/repro.php or contact Special Collections at speccoll(at)umbc.edu
This item may be protected under Title 17 of the U.S. Copyright Law. It is made available by UMBC for non-commercial research and education. For permission to publish or reproduce, please see http://aok.lib.umbc.edu/specoll/repro.php or contact Special Collections at speccoll(at)umbc.edu
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Abstract
Lethal human prostate cancer (PCa) frequently harbors MYC gain-of-function and PTEN loss-of-function. In the BMPCFVB mouse model of PCa (Hoxb13-MYC;Hoxb13-Cre;Ptenfl/fl), concurrent genetic deletion of mouse Pten and overexpression of human MYC were sufficient to promote rapid neoplastic growth and metastasis with high penetrance. We hypothesized that breeding the BMPCFVB transgenes onto the C57BL/6J (B6) genetic background would result in slower PCa kinetics. Transgenic offspring with the highest B6 genomic content, determined by genomic SNP and SSLP analyses, were selected for further backcrossing. Our preliminary data suggest that BMPCB6 tumorigenesis involves early-onset and prolonged inflammation, complete penetrance of cystic anterior prostates, and slower and/or multiphase progression as compared to that in the BMPCFVB model. Importantly, BMPCB6 mice develop adenocarcinoma and lymph node metastases histologically similar to BMPCFVB tumors. These data will facilitate future studies aiming to examine strain-dependent differences in tumorigenesis and determine mechanisms underlying PCa resistance in the B6 strain.