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The hD52 ( TPD52 ) gene is a candidate target gene for events resulting in increased 8q21 copy number in human breast carcinoma
Author(s) -
Balleine Rosemary L.,
Fejzo Marlena Schoenberg,
Sathasivam Pavani,
Basset Paul,
Clarke Christine L.,
Byrne Jennifer A.
Publication year - 2000
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/1098-2264(2000)9999:9999<::aid-gcc1005>3.0.co;2-o
Subject(s) - breast carcinoma , amplicon , breast cancer , gene , biology , locus (genetics) , gene dosage , gene expression , chromosome 17 (human) , correlation , copy number variation , chromosome , cancer research , oncology , genetics , cancer , medicine , polymerase chain reaction , geometry , mathematics , genome
Chromosome band 8q21 is frequently overrepresented in human cancer, but to date no 8q21 target gene has been proposed. The hD 52 ( TPD 52) gene is of potential significance in breast and other cancers due to its location and expression pattern. Fine mapping of hD 52 placed this locus within the peak of the 8q21 amplicon delineated in the SK‐BR‐3 breast carcinoma cell line, and a positive association between hD 52 gene dosage and transcript levels was subsequently demonstrated in four breast carcinoma cell lines, including SK‐BR‐3. Increased copy number (ICN) was measured using Southern blot analyses in 3/32 human breast carcinomas at hD 52, and the related hD 54 gene in 20q13.2–q13.3. Subsequent immunohistochemical analysis of hD52 expression in 19 breast carcinomas with varying hD 52 gene dosages demonstrated a significant positive association between hD 52 dosage and hD52 expression using a Spearman rank correlation coefficient (r s = 0.573, α = 0.01) and a Wilcoxon rank‐sum test (α = 0.05). On the basis of its map location and expression pattern in breast carcinoma, we therefore propose hD 52 as a candidate target gene at chromosome band 8q21. Genes, Chromosomes and Cancer 29:48–57, 2000. © 2000 Wiley‐Liss, Inc.