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Phenotypes Associated with This Genotype
Genotype
MGI:5543907
Allelic
Composition
Braftm1Mmcm/Braftm1Mmcm
Nkx3-1tm4(cre/ERT2)Mms/Nkx3-1+
Ptentm1Hwu/Pten+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (2 available); any Braf mutation (13 available)
Nkx3-1tm4(cre/ERT2)Mms mutation (1 available); any Nkx3-1 mutation (20 available)
Ptentm1Hwu mutation (3 available); any Pten mutation (39 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• mutants develop lethal prostate cancer 4 months after tamoxifen induction
• tumors are large and highly proliferative and are primarily composed of luminal epithelial cells
• tamoxifen treated mutants do not display significant tumor regression at 2 weeks following castration, indicating that tumors are resistant to castration
• tumors from tamoxifen treated mutants show absence of cellular senescence and are highly proliferative
• treatment of tamoxifen treated mutants with a combination of rapamycin and PD0325901 (a mitogen-activated protein/extracellular signal-regulated kinase inhibitor) results in a reduction in tumor weight, growth, and proliferation
• tamoxifen treated mutants develop invasive adenocarcinoma by 2-3 months after tamoxifen induction
• tamoxifen treated mutants display prostate intraepithelial neoplasia (PIN) by 2-4 weeks after tamoxifen induction

endocrine/exocrine glands
• mutants develop lethal prostate cancer 4 months after tamoxifen induction
• tumors are large and highly proliferative and are primarily composed of luminal epithelial cells
• tamoxifen treated mutants do not display significant tumor regression at 2 weeks following castration, indicating that tumors are resistant to castration
• tumors from tamoxifen treated mutants show absence of cellular senescence and are highly proliferative
• treatment of tamoxifen treated mutants with a combination of rapamycin and PD0325901 (a mitogen-activated protein/extracellular signal-regulated kinase inhibitor) results in a reduction in tumor weight, growth, and proliferation
• tamoxifen treated mutants develop invasive adenocarcinoma by 2-3 months after tamoxifen induction
• tamoxifen treated mutants display prostate intraepithelial neoplasia (PIN) by 2-4 weeks after tamoxifen induction

mortality/aging
• mutants develop lethal prostate cancer 4 months after tamoxifen induction

neoplasm
• mutants develop lethal prostate cancer 4 months after tamoxifen induction
• tumors are large and highly proliferative and are primarily composed of luminal epithelial cells
• tamoxifen treated mutants do not display significant tumor regression at 2 weeks following castration, indicating that tumors are resistant to castration
• tumors from tamoxifen treated mutants show absence of cellular senescence and are highly proliferative
• treatment of tamoxifen treated mutants with a combination of rapamycin and PD0325901 (a mitogen-activated protein/extracellular signal-regulated kinase inhibitor) results in a reduction in tumor weight, growth, and proliferation
• tamoxifen treated mutants develop invasive adenocarcinoma by 2-3 months after tamoxifen induction
• tamoxifen treated mutants display prostate intraepithelial neoplasia (PIN) by 2-4 weeks after tamoxifen induction
• metastases to lungs and lymph nodes are seen in tamoxifen treated mutants and disseminated tumor cells are seen in the bone marrow


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
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last database update
10/08/2019
MGI 6.14
The Jackson Laboratory