Bieberich, Charles JChin, Alexander2022-02-092022-02-092020-01-0112368http://hdl.handle.net/11603/24204Lethal 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.application:pdfC57BL/6FVBmetastasisMYCProstate cancerPTENEffect of genetic background on the initiation and progression of mouse prostate cancer driven by MYC overexpression and Pten lossText