title: Visualization of INT2 and HST1 amplification in oral squamous cell carcinomas.
abstract: Oral squamous cell carcinoma (OSCC) develops along a multistep genetic pathway including loss of tumor suppressor genes and alteration of oncogenes. We characterized seven OSCC cell lines by classical and molecular cytogenetic analysis and fresh tumor and adjacent oral mucosa corresponding to three of the cell lines by molecular cytogenetics. We observed homogeneously staining regions (hsrs) in four of the seven cell lines, at 11q13 in three and at 11q23 and in an unidentified marker chromosome in the fourth. Amplification of band 11q13 occurs in 30-60% of head and neck squamous cell carcinomas. To determine whether INT2 and HST1, both located in band 11q13, are amplified in the tissues and cell lines and to confirm the chromosomal location(s) of the amplification, we used dual-color fluorescence in situ hybridization (FISH) with DNA probes for these genes and the chromosome 11 centromere. We report chromosomal localization of INT2/HST1 amplification in OSCC. Coamplification of INT2 and HST1 was detected in the hsrs in cultured tumor cells from the four hsr-containing tumors and in directly harvested tumor cells, which were available from only two of these tumors. Amplification was not present in tumors lacking hsrs or adjacent oral mucosa corresponding to any of the seven tumors. The observation of amplification in fresh tumor cells suggests that the amplification was present in the patients, may play a key role in the development and/or progression of OSCC, and is not due to karyotypic evolution in vitro. The absence of amplification in the adjacent mucosa suggests that 11q13 amplification is a relatively late event in OSCC tumorigenesis.
authors.affiliation: Department of Human Genetics, University of Pittsburgh, Pennsylvania, USA.
authors.forename: C M
authors.initials: CM
authors.lastname: Lese
authors.forename: K M
authors.initials: KM
authors.lastname: Rossie
authors.forename: B N
authors.initials: BN
authors.lastname: Appel
authors.forename: J K
authors.initials: JK
authors.lastname: Reddy
authors.forename: J T
authors.initials: JT
authors.lastname: Johnson
authors.forename: E N
authors.initials: EN
authors.lastname: Myers
authors.forename: S M
authors.initials: SM
authors.lastname: Gollin
mesh_terms: D001706:Biopsy; D002294:Carcinoma, Squamous Cell / Q000235:genetics* / Q000473:pathology; D002460:Cell Line; D002869:Chromosome Aberrations; D002874:Chromosome Mapping; D002880:Chromosomes, Human, Pair 11; D051518:Fibroblast Growth Factor 3; D051519:Fibroblast Growth Factor 4; D005346:Fibroblast Growth Factors / Q000096:biosynthesis / Q000235:genetics*; D005784:Gene Amplification; D006258:Head and Neck Neoplasms / Q000235:genetics; D006801:Humans; D007621:Karyotyping; D009061:Mouth Mucosa / Q000473:pathology; D009062:Mouth Neoplasms / Q000235:genetics* / Q000473:pathology; D011505:Protein-Tyrosine Kinases / Q000235:genetics; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis / Q000235:genetics*
chemical_list: C496444:FGF3 protein, human; C496445:FGF4 protein, human; D051518:Fibroblast Growth Factor 3; D051519:Fibroblast Growth Factor 4; D011518:Proto-Oncogene Proteins; D005346:Fibroblast Growth Factors; D011505:Protein-Tyrosine Kinases