Abstract：
:Hormonal, genetic, and environmental factors play major roles in the complex etiology of breast cancer. When treated continuously with 17beta-estradiol (E2), the ACI rat exhibits a genetically conferred propensity to develop mammary cancer. The susceptibility of the ACI rat to E2-induced mammary cancer appears to segregate as an incompletely dominant trait in crosses to the resistant Copenhagen (COP) strain. In both (ACI x COP)F(2) and (COP x ACI)F(2) populations, we find strong evidence for a major genetic determinant of susceptibility to E2-induced mammary cancer on distal rat chromosome 5. Our data are most consistent with a model in which the ACI allele of this locus, termed Emca1 (estrogen-induced mammary cancer 1), acts in an incompletely dominant manner to increase both tumor incidence and tumor multiplicity as well as to reduce tumor latency in these populations. We also find evidence suggestive of a second locus, Emca2, on chromosome 18 in the (ACI x COP)F(2) population. The ACI allele of Emca2 acts in a dominant manner to increase incidence and decrease latency. Together, Emca1 and Emca2 act independently to modify susceptibility to E2-induced mammary cancer.
journal_name
Geneticsjournal_title
Geneticsauthors
Gould KA,Tochacek M,Schaffer BS,Reindl TM,Murrin CR,Lachel CM,VanderWoude EA,Pennington KL,Flood LA,Bynote KK,Meza JL,Newton MA,Shull JDdoi
10.1534/genetics.104.033878keywords:
subject
Has Abstractpub_date
2004-12-01 00:00:00pages
2113-25issue
4eissn
0016-6731issn
1943-2631pii
168/4/2113journal_volume
168pub_type
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