FHIT gene alterations in head and neck squamous cell carcinomas.
Author(s) -
Laura Virgilio,
Michèle Shuster,
Susanne M. Gollin,
M L Veronese,
Masataka Ohta,
Kay Huebner,
C M Croce
Publication year - 1996
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.93.18.9770
Subject(s) - fhit , locus (genetics) , biology , head and neck squamous cell carcinoma , loss of heterozygosity , fluorescence in situ hybridization , gene , allele , cancer research , microbiology and biotechnology , cell , epidermoid carcinoma , exon , chromosomal fragile site , genetics , tumor suppressor gene , carcinogenesis , chromosome , cancer , head and neck cancer
To determine whether the FHIT gene at 3p14.2 is altered in head and neck squamous cell carcinomas (HNSCC), we examined 26 HNSCC cell lines for deletions within the FHIT locus by Southern analysis, for allelic losses of specific exons FHIT by fluorescence in situ hybridization (FISH) and for integrity of FHIT transcripts. Three cell lines exhibited homozygous deletions within the FHIT gene, 55% (15/25) showed the presence of aberrant transcripts, and 65% (13/20) showed the presence of multiple cell populations with losses of different portions of FHIT alleles by FISH of FHIT genomic clones to interphase nuclei. When the data obtained by FISH and by reverse transcriptase-PCR analyses are combined, 22 of 26 cell lines showed alterations of at least one allele of the FHIT gene. Our data indicate that the FHIT gene is disrupted in HNSCCs and hence, loss of FHIT function may be important in the development and/or progression of head and neck cancers.
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