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• W2103856988 abstract "The majority of human breast cancers are estrogen receptor-positive (ER+), but this has proven challenging to model in genetically engineered mice. This review summarizes information on 21 mouse models that develop ER+ mammary cancer. Where available, information on cancer pathology and gene expression profiles is referenced to assist in understanding which histological subtype of ER+ human cancer each model might represent. ESR1 , CCDN1 , prolactin, TGFα , AIB1 , ESPL1 , and WNT1 overexpression, PIK3CA gain of function, as well as loss of P53 ( Trp53 ) or STAT1 are associated with ER+ mammary cancer. Treatment with the PPARγ agonist efatutazone in a mouse with Brca1 and p53 deficiency and 7,12-dimethylbenz(a)anthracene exposure in combination with an activated myristoylated form of AKT1 also induce ER+ mammary cancer. A spontaneous mutant in nude mice that develops metastatic ER+ mammary cancer is included. Age of cancer development ranges from 3 to 26 months and the percentage of cancers that are ER+ vary from 21 to 100%. Not all models are characterized as to their estrogen dependency and/or response to anti-hormonal therapy. Strain backgrounds include C57Bl/6, FVB, BALB/c, 129S6/SvEv, CB6F1, and NIH nude. Most models have only been studied on one strain background. In summary, while a range of models are available for studies of pathogenesis and therapy of ER+ breast cancers, many could benefit from further characterization, and opportunity for development of new models remains." @default.
• W2103856988 created "2016-06-24" @default.
• W2103856988 creator A5022334540 @default.
• W2103856988 creator A5053625755 @default.
• W2103856988 date "2014-01-30" @default.
• W2103856988 modified "2023-10-10" @default.
• W2103856988 title "Genetically engineered ERα-positive breast cancer mouse models" @default.
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