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Relationship between FRA11F and 11q13 gene amplification in oral cancer
Author(s) -
Reshmi Shalini C.,
Huang Xin,
Schoppy David W.,
Black Robert C.,
Saunders William S.,
Smith David I.,
Gollin Susanne M.
Publication year - 2007
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/gcc.20394
Subject(s) - gene duplication , chromosomal fragile site , biology , amplicon , loss of heterozygosity , fluorescence in situ hybridization , chromosomal translocation , gene , microbiology and biotechnology , genetics , polymerase chain reaction , chromosome , allele
Common fragile sites (CFS) are nonstaining gaps or breaks in chromosomes that are expressed under conditions inducing replicative stress. CFS have been suggested to play a role in epithelial cancers by their association with loss of heterozygosity, loss of gene expression, and/or gene amplification in the form of homogeneously staining regions (hsrs). In oral squamous‐cell carcinomas (OSCC), amplification of chromosomal band 11q13 occurs in the form of an hsr. We suggested previously that CFS flanking 11q13 may be susceptible to breakage induced by tobacco or other carcinogens and/or human papillomavirus, promoting formation of the 11q13 amplicon. Examination of OSCC cell lines with 11q13 amplification using fluorescence in situ hybridization showed loss of FRA11F sequences, whereas cell lines without 11q13 amplification displayed an intact FRA11F site. Cell lines with more complex 11q rearrangements expressed FRA11F in the form of an inverted duplication, characteristic of breakage‐fusion‐bridge cycles. Our findings suggest that gene amplification involving chromosomal band 11q13 in OSCC may be initiated by breakage at FRA11F . © 2006 Wiley‐Liss, Inc.