Oral squamous cell carcinomas are characterized by a rather uniform pattern of genomic imbalances detected by comparative genomic hybridisation

Wolff, E; Girod, Sabine; Liehr, Thomas; Vorderwülbecke, U.; Ries, Jutta; Steininger, H; Gebhart, Erich

doi:10.1016/s1368-8375(97)00079-1

Cited by 67 publications

(55 citation statements)

References 15 publications

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“…Since the most common genetic aberrations had already been detected in OSCC cell lines and primary tumors by conventional CGH (Hermsen et al, 1997;Wolff et al, 1998), here, we paid attention to more remarkable patterns of chromosomal abnormalities, such as highlevel amplifications and homozygous deletions, which are likely to be landmarks of oncogenes and TSGs, respectively (Baldwin et al, 2005;Snijders et al, 2005). Tables 1 and 2 summarize the clones showing high-level amplifications (log 2 ratio >2.0) or homozygous deletions (log 2 ratiooÀ2.0), respectively.…”

Section: Resultsmentioning

confidence: 99%

PRTFDC1, a possible tumor-suppressor gene, is frequently silenced in oral squamous-cell carcinomas by aberrant promoter hypermethylation

et al. 2007

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Array-based comparative genomic hybridization (array-CGH) has good potential for the high-throughput identification of genetic aberrations in cell genomes. In the course of a program to screen a panel of oral squamouscell carcinoma (OSCC), cell lines for genomic copynumber aberrations by array-CGH using our in-house arrays, we identified a 3-Mb homozygous deletion at 10p12 in 1 of 18 cell lines (5.6%). Among seven genes located within this region, expression of PRTFDC1 mRNA was not detected in 50% (9/18) or decreased in 5.6% (1/18) of OSCC cell lines, but detected in normal oral epithelia and restored in gene-silenced OSCC cells without its homozygous loss after treatment with 5-aza-2 0 -deoxycytidine. Among 17 cell lines without a homozygous deletion, the hypermethylation of the PRTFDC1 CpG island, which showed promoter activity, was observed in all nine cell lines with no or reduced PRTFDC1 expression (52.9%). Methylation of this CpG island was also observed in primary OSCC tissues (8/47, 17.0%). In addition, restoration of PRTFDC1 in OSCC cells lacking its expression inhibited cell growth in colony-formation assays, whereas knockdown of PRTFDC1 expression in OSCC cells expressing the gene promoted cell growth. These results suggest that epigenetic silencing of PRTFDC1 by hypermethylation of the CpG island leads to a loss of PRTFDC1 function, which might be involved in squamous cell oral carcinogenesis.

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Section: Resultsmentioning

confidence: 99%

PRTFDC1, a possible tumor-suppressor gene, is frequently silenced in oral squamous-cell carcinomas by aberrant promoter hypermethylation

et al. 2007

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“…The amplification at 3q has been detected in ESC 18) and other types of tumor such as ovarian cancer, 27) and squamous cell carcinoma (SCC) of the lung, 28) and head and neck including oral cavity. 29) The possible candidate genes involved in tumor development include the genes for ribosomal protein L22 (RPL22), butyrylcholinesterase (BCHE), glucose transporter 2 (SLC2A2), transferrin receptor (TFRC), thrombopoietin (THPO) and the phosphatidylinositol-3 kinase catalytic α polypeptide (PIK3CA). The combined amplification and expression of these genes in SCC in several organs raise the possibility that several amplified and functionally important genes at 3q26 may be involved in the pathogenesis of SCC, especially lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Nonrandom Chromosomal Imbalances in Esophageal Squamous Cell Carcinoma Cell Lines: Possible Involvement of the ATF3 and CENPF Genes in the 1q32 Amplicon

Pimkhaokham

Shimada

Fukuda

et al. 2000

Japanese Journal of Cancer Research

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Using comparative genomic hybridization (CGH), we investigated copy number aberrations in 29 esophageal squamous cell carcinoma (ESC) cell lines. All lines displayed numerous chromosome imbalances. The most frequent losses were observed on chromosome 18q (65.5%), Xp (48.3%), 3p (44.8%), 4q (44.8%), 8p (41.4%), 11q23-25 (34.5%) and 4p (27.6%), whereas the most common copy number gains were noted at 8q (86.2%), 3q (82.8%), 5p (69%), 7p (69%), 20q (65.5%), 9q (55.2%), 11q (55.2%), 1q (48.3%), Xq (44.8%) and 18p (37.9%). High-level gains (HLGs) were detected at 3q26 (9 cases), 8q23 (6 cases), 5p14-15 (6 cases), 18p11.2-11.3 (6 cases), 3q27-28 (5 cases), 5p13 (3 cases), 7p14-15 (3 cases), 20q12-13 (3 cases), 11q13 (3 cases), 14q21 (2 cases), 20p11.2 (2 cases), 13q32 (2 case), and 1q32 (1 case). Among them, HLGs of 1q32 have been reported in other types of cancer, including glioblastoma and breast cancers. We successfully narrowed down the smallest common amplicon involving 1q-gain to the genomic segment between D1S414 and D1S2860 by fluorescence in situ hybridization (FISH). Southern and northern blot analysis clearly demonstrated that ATF3, human activating transcription factor-3 and CENPF, centromere protein F, mapped within this region, were significantly amplified and over-expressed in 1q32 amplicon.

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“…Because loss of chromosomal arm 3p has been well characterized in head and neck cancer by using CGH (3)(4)(5)(6)(7)(8)19) and minimal areas of loss further detailed using microsatellite analysis (17,18,26), a smaller regional analysis of 3p was performed to identify specific areas of underexpression. A similar analysis was done for chromosomal arm 22q to identify regions with significant overexpression.…”

Section: Methodsmentioning

confidence: 99%

“…Chronic exposure of the upper aeorodigestive tract to known carcinogens in alcohol and tobacco ultimately results in the accumulation of multiple genetic aberrations in exposed mucosa (3). Genetic events involved in head and neck carcinogenesis have been characterized by using techniques including microsatellite analysis and comparative genomic hybridization (CGH) (3)(4)(5)(6)(7)(8), whereas transcriptional alterations have been characterized by using several techniques, including gene expression profiling based on microarray technology (9,10).…”

mentioning

confidence: 99%

Gene expression alterations over large chromosomal regions in cancers include multiple genes unrelated to malignant progression

Masayesva

Garrett‐Mayer

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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In solid tumors, the relationship between DNA copy number and global expression over large chromosomal regions has not been systematically explored. We used a 12,626-gene expression array analysis of head and neck squamous cell carcinoma and normal oral mucosa and annotated gene expression levels to specific chromosomal loci. Expression alterations correlated with reported data using comparative genomic hybridization. When genes with significant differences in expression between normal and malignant lesions, as defined by significance analysis of microarrays (SAM), were compared to nonsignificant genes, similar chromosomal patterns of alteration in expression were noted. Individual tumors underwent microsatellite analysis and 2 analysis of expression at 3p and 22q. Significant 3p underexpression and 22q overexpression were found in all primary tumors with 3p and 22q allelic imbalance, respectively, whereas no tumor without allelic imbalance on these chromosomal arms demonstrated expression differences. Loss and gain of chromosomal material in solid cancers can alter gene expression over large chromosomal regions, including multiple genes unrelated to malignant progression. chromosomal mapping ͉ microarrays ͉ comparative genomic hybridization ͉ allelic imbalance ͉ head and neck squamous cell carcinoma

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Oral squamous cell carcinomas are characterized by a rather uniform pattern of genomic imbalances detected by comparative genomic hybridisation

Cited by 67 publications

References 15 publications

PRTFDC1, a possible tumor-suppressor gene, is frequently silenced in oral squamous-cell carcinomas by aberrant promoter hypermethylation

PRTFDC1, a possible tumor-suppressor gene, is frequently silenced in oral squamous-cell carcinomas by aberrant promoter hypermethylation

Nonrandom Chromosomal Imbalances in Esophageal Squamous Cell Carcinoma Cell Lines: Possible Involvement of the ATF3 and CENPF Genes in the 1q32 Amplicon

Gene expression alterations over large chromosomal regions in cancers include multiple genes unrelated to malignant progression

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