All Phenotypes Tg(tetO-BRAF*V600E)29Lc MGI Mouse

mortality/aging

premature death ( J:144358 )

• 50% of doxycycline-treated mice die due to generally compromised physiological state secondary to renal failure despite frequent bladder irrigations

neoplasm

increased prostate gland adenocarcinoma incidence ( J:144358 )

• at 24 weeks after doxycycline induction, mice develop prostate adenocarcinomas that exhibit epithelial-mesenchyme transition

• doxycycline-induced prostate adenomas can compress the bladder, originate from epithelial cells and express luminal, intermediate and basal cell markers

• doxycycline-treated mice that are subsequently castrated exhibit reduced prostate tumor proliferation compared to pre-castration

• withdrawal of doxycycline does not affect tumor cell proliferation

endocrine/exocrine glands

prostate gland hyperplasia ( J:144358 )

• at 16 weeks after doxycycline induction, prostates exhibit basaloid hyperplasia driven by urogenital epithelium unlike in wild-type mice

increased prostate gland adenocarcinoma incidence ( J:144358 )

• at 24 weeks after doxycycline induction, mice develop prostate adenocarcinomas that exhibit epithelial-mesenchyme transition

• doxycycline-induced prostate adenomas can compress the bladder, originate from epithelial cells and express luminal, intermediate and basal cell markers

• doxycycline-treated mice that are subsequently castrated exhibit reduced prostate tumor proliferation compared to pre-castration

• withdrawal of doxycycline does not affect tumor cell proliferation

abnormal prostate gland physiology ( J:144358 )

• at 5 weeks after doxycycline induction, prostates exhibit a moderate degree of aberrant proliferation unlike in wild-type mice

reproductive system

prostate gland hyperplasia ( J:144358 )

• at 16 weeks after doxycycline induction, prostates exhibit basaloid hyperplasia driven by urogenital epithelium unlike in wild-type mice

increased prostate gland adenocarcinoma incidence ( J:144358 )

• at 24 weeks after doxycycline induction, mice develop prostate adenocarcinomas that exhibit epithelial-mesenchyme transition

• doxycycline-induced prostate adenomas can compress the bladder, originate from epithelial cells and express luminal, intermediate and basal cell markers

• doxycycline-treated mice that are subsequently castrated exhibit reduced prostate tumor proliferation compared to pre-castration

• withdrawal of doxycycline does not affect tumor cell proliferation

abnormal prostate gland physiology ( J:144358 )

• at 5 weeks after doxycycline induction, prostates exhibit a moderate degree of aberrant proliferation unlike in wild-type mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
prostate cancer		DOID:10283	OMIM:176807 OMIM:300147 OMIM:300704 OMIM:601518 OMIM:602759 OMIM:608656 OMIM:608658 OMIM:609299 OMIM:609558 OMIM:610321 OMIM:610997 OMIM:611100 OMIM:611868 OMIM:611928 OMIM:611955 OMIM:611958 OMIM:611959	J:144358

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

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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