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Nonrandom pattern of aberrations in 17β-estradiol-induced rat mammary tumors: Indications of distinct pathways for tumor development
Högskolan i Skövde, Institutionen för teknik och samhälle.
CMB-Genetics, Göteborg University, SE 40530 Göteborg, Sweden / Department of Clinical Genetics, Göteborg University, SE 40530 Göteborg, Sweden.
Högskolan i Skövde, Institutionen för kommunikation och information.
Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, NE 68198, United States / Eppley Institute for Research in Cancer, University of Nebraska Medical Center, Omaha, NE 68198, United States.
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2007 (engelsk)Inngår i: Genes, Chromosomes and Cancer, ISSN 1045-2257, E-ISSN 1098-2264, Vol. 46, nr 5, s. 459-469Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Estrogens play an important role in breast cancer etiology and the ACI rat provides a novel animal model for defining the mechanisms through which estrogens contribute to mammary cancer development. In crossing experiments between the susceptible ACI strain and two resistant strains, COP (Copenhagen) and BN (Brown Norway), several quantitative trait loci (QTL) that affect development of 17b-estradiol (E2)-induced mammary tumors have been defined. Using comparative genomic hybridization (CGH), we have analyzed cytogenetic aberrations in E2-induced mammary cancers and have found clear patterns of nonrandom chromosomal involvement. Approximately two thirds of the tumors exhibited copy number changes. Losses of rat chromosome 5 (RNO5) and RNO20 were particularly common, and it was found that these two aberrations often occurred together. A third recurrent aberration involving proximal gain and distal loss in RNO6 probably defined a distinct subgroup of tumors, since it never occurred in combination with RNO5 loss. Interestingly, QTL with powerful effects on mammary cancer development have been mapped to RNO5 and RNO6. These findings suggest that there were at least two genetic pathways to tumor formation in this rat model of E2-induced mammary cancer. By performing CGH on mammary tumors from ACI rats, F1 rats from crosses between the ACI and COP or BN strains and ACI.BN-Emca8 congenic rats, which carry the BN allele of the Emca8 QTL on RNO5 on the ACI genetic background, we were able to determine that the constitution of the germ line influences the pattern of chromosomal aberrations.

sted, utgiver, år, opplag, sider
Wiley-Liss, Inc. , 2007. Vol. 46, nr 5, s. 459-469
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URN: urn:nbn:se:his:diva-1991DOI: 10.1002/gcc.20428ISI: 000244904500005PubMedID: 17285573Scopus ID: 2-s2.0-33947397961OAI: oai:DiVA.org:his-1991DiVA, id: diva2:32267
Merknad

Tatjana Adamovic

CMB-Genetics, Göteborg University, SE 40530 Göteborg,SwedenDepartmentof Clinical Genetics, Göteborg University, SE 40530 Göteborg, Sweden

Tilgjengelig fra: 2008-04-18 Laget: 2008-04-18 Sist oppdatert: 2017-12-12bibliografisk kontrollert

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