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Visualization of INT2 and HST1 Amplification in oral squamous cell carcinomas
Author(s) -
Lese Christa M.,
Rossie Karen M.,
Appel Billy N.,
Reddy Jaya K.,
Johnson Jonas T.,
Myers Eugene N.,
Gollin Susanne M.
Publication year - 1995
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.2870120409
Subject(s) - fluorescence in situ hybridization , molecular cytogenetics , gene duplication , oral mucosa , comparative genomic hybridization , pathology , karyotype , chromosome , cell culture , cell , in situ hybridization , cytogenetics , basal cell , microbiology and biotechnology , biology , cancer research , gene , medicine , genetics , gene expression
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.