The A4396G polymorphism in interferon regulatory factor 1 is frequently expressed in breast cancer cell lines

Kerrie B. Bouker, Todd Skaar, David S. Harburger, Rebecca B. Riggins, David R. Fernandez, Alan Zwart, Robert Clarke

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Loss or mutation of known tumor suppressor genes accounts for a small proportion of all breast cancers. We have recently shown that interferon regulatory factor 1 (IRF1) is a putative tumor suppressor gene in breast cancer. We now report that the A4396G single nucleotide polymorphism in the IRF1 gene is more frequent in human breast cancer cell lines than in the general population (P = 0.01). Furthermore, A4396G is more frequently expressed in African American (black) than in European ancestry (white) subjects (n = 70 subjects; P ≤ 0.001), leading to a significant difference in genotype distribution between these populations (P = 0.002).

Original languageEnglish (US)
Pages (from-to)61-64
Number of pages4
JournalCancer Genetics and Cytogenetics
Volume175
Issue number1
DOIs
StatePublished - May 2007
Externally publishedYes

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Interferon Regulatory Factor-1
Breast Neoplasms
Tumor Suppressor Genes
Cell Line
African Americans
Single Nucleotide Polymorphism
Genotype
Demography
Mutation
Population
Genes

ASJC Scopus subject areas

  • Cancer Research
  • Genetics
  • Molecular Biology

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The A4396G polymorphism in interferon regulatory factor 1 is frequently expressed in breast cancer cell lines. / Bouker, Kerrie B.; Skaar, Todd; Harburger, David S.; Riggins, Rebecca B.; Fernandez, David R.; Zwart, Alan; Clarke, Robert.

In: Cancer Genetics and Cytogenetics, Vol. 175, No. 1, 05.2007, p. 61-64.

Research output: Contribution to journalArticle

Bouker, Kerrie B. ; Skaar, Todd ; Harburger, David S. ; Riggins, Rebecca B. ; Fernandez, David R. ; Zwart, Alan ; Clarke, Robert. / The A4396G polymorphism in interferon regulatory factor 1 is frequently expressed in breast cancer cell lines. In: Cancer Genetics and Cytogenetics. 2007 ; Vol. 175, No. 1. pp. 61-64.
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