Normal breast growth and development depends on functional androgen:estrogen (A:E) balance. Androgen actions are mediated by the androgen receptor (AR), a DNA-binding, transcriptional-regulatory protein. Decreased AR transactivational. activity lowers A:E balance and may result in functional hyperestrogenicity: this could promote the pathogenesis of breast cancer (BC). The present study is the first to seek AR mutations in female BC. The length of the polymorphic CAG-repeat in exon 1 of the AR correlates inversely with the transactivational activity of the AR. Using 10% polyacrylamide gels, I found a significant (p < 0.0001) shift to greater CAG-repeat lengths in BC samples. This suggests a role for ARs with long polyglutamine tracts in the initiation and/or progression of BC. Exons 2--8 of the AR in 81 fresh frozen BC tumor tissues were screened for mutations using SSCP analysis. I did not detect any mutations in these exons.
Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.20255 |
Date | January 1997 |
Creators | Elhaji, Youssef A. |
Publisher | McGill University |
Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
Language | English |
Detected Language | English |
Type | Electronic Thesis or Dissertation |
Format | application/pdf |
Coverage | Master of Science (Department of Biology.) |
Rights | All items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated. |
Relation | alephsysno: 001609634, proquestno: MQ44162, Theses scanned by UMI/ProQuest. |
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