About   Help   FAQ
Phenotypes Associated with This Genotype
Genotype
MGI:3843497
Allelic
Composition
Cav1tm1Mls/Cav1tm1Mls
Genetic
Background
involves: 129/Sv * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cav1tm1Mls mutation (2 available); any Cav1 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• ovariectomized female mice exposed to estrogen exhibit a 2-fold increase in ductal thickening and extensive side-branching compared to similarly treated wild-type mice
• estrogen-induced secondary branching is 3- to 4-fold greater and tertiary branching 5- to 7-fold greater than in similarly treated wild-type mice
• female mice exposed to high levels of estrogen develop abnormal mammary lesions or focal dysplasia unlike similarly treated wild-type mice with a 4-fold increase in lesion frequency and a 2.5-fold increase in lesion diameter
• estrogen-treated mice develop ductal carcinoma in situ in the mammary glands unlike similarly treated wild-type mice
• estrogen-treated lesions exhibit nuclear atypia and heterogeneity, complete filling of ductal lumens, and local infiltration with small blood vessels
• ductal lesions in estrogen-treated mice exhibit abnormal distribution of myoepithelial cells, increased cell proliferation at terminal end buds, stromal activation, and enriched in mammary stem/progenitor cells
• ductal lesions in estrogen treated mice express Npm1 (B23), a marker for tamoxifen resistance, and Nol3 (Arc), a marker of resistance to apoptosis

neoplasm
• estrogen-treated mice develop ductal carcinoma in situ in the mammary glands unlike similarly treated wild-type mice
• estrogen-treated lesions exhibit nuclear atypia and heterogeneity, complete filling of ductal lumens, and local infiltration with small blood vessels
• ductal lesions in estrogen-treated mice exhibit abnormal distribution of myoepithelial cells, increased cell proliferation at terminal end buds, stromal activation, and enriched in mammary stem/progenitor cells
• ductal lesions in estrogen treated mice express Npm1 (B23), a marker for tamoxifen resistance, and Nol3 (Arc), a marker of resistance to apoptosis

integument
• ovariectomized female mice exposed to estrogen exhibit a 2-fold increase in ductal thickening and extensive side-branching compared to similarly treated wild-type mice
• estrogen-induced secondary branching is 3- to 4-fold greater and tertiary branching 5- to 7-fold greater than in similarly treated wild-type mice
• female mice exposed to high levels of estrogen develop abnormal mammary lesions or focal dysplasia unlike similarly treated wild-type mice with a 4-fold increase in lesion frequency and a 2.5-fold increase in lesion diameter
• estrogen-treated mice develop ductal carcinoma in situ in the mammary glands unlike similarly treated wild-type mice
• estrogen-treated lesions exhibit nuclear atypia and heterogeneity, complete filling of ductal lumens, and local infiltration with small blood vessels
• ductal lesions in estrogen-treated mice exhibit abnormal distribution of myoepithelial cells, increased cell proliferation at terminal end buds, stromal activation, and enriched in mammary stem/progenitor cells
• ductal lesions in estrogen treated mice express Npm1 (B23), a marker for tamoxifen resistance, and Nol3 (Arc), a marker of resistance to apoptosis

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
breast cancer DOID:1612 OMIM:114480
J:147439


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)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
03/12/2024
MGI 6.23
The Jackson Laboratory