Rare amplicons implicate frequent deregulation of cell fate specification pathways in oral squamous cell carcinoma

Snijders, Antoine M.; Schmidt, Brian L.; Fridlyand, Jane; Dekker, Nusi P.; Pinkel, Daniel; Jordan, Richard C.; Albertson, Donna G.

doi:10.1038/sj.onc.1208601

Cited by 245 publications

(223 citation statements)

References 48 publications

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“…In addition, many identified genes which have been reported as cancer-associated genes. For example, the up-expression of cyclin D3 gene in liver metastasis of colorectal cancer [10], matrix metallopeptidase 7 in oral squamous cell carcinoma [11], and regulator of G-protein signaling 5 in RCC [12] were observed and they were also identified as up-regulated genes in this study. Furthermore, the association of the apoptosis-related gene kininogen 1 [13] and the cytoskeleton-related gene gelsolin [14] with cancer were previously reported and the down-regulation of kininogen 1 and gelsolin in ccRCC tissues was also found in this study.…”

Section: Functional Classification Of the Differentially Expressed Genessupporting

confidence: 56%

Identification of differentially expressed genes in clear cell renal cell carcinoma by analysis of full-length enriched cDNA library

et al. 2006

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SummaryRenal cell carcinoma (RCC) is the most common malignancy in adult kidney, and accounts for 3% of malignancies worldwide with increasing incidence. Clear cell RCC (ccRCC) is the major type in RCC. Resection by surgery is the main treatment because the response of ccRCC to traditional therapies is very poor. To identify the tumor-associated genes for better understanding the molecular mechanism of ccRCC, the full-length enriched cDNA libraries of ccRCC and normal kidney tissues were constructed by the oligo-capping method. Nucleotide sequences of the cDNA libraries of ccRCC and normal kidney tissues were sequenced. From the sequence analysis of 19,425 and 12,400 clones of ccRCC and normal kidney tissues, 4356 and 3055 genes were identified, respectively. By comparing the gene-expression patterns of ccRCC and normal tissues, the up-or down-regulated genes were identified. Among these identified genes, the differential expression of annexin A2 and argininosuccinate synthetase genes were further confirmed by quantitative real-time PCR and Western blot analysis.

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Section: Functional Classification Of the Differentially Expressed Genessupporting

confidence: 56%

Identification of differentially expressed genes in clear cell renal cell carcinoma by analysis of full-length enriched cDNA library

et al. 2006

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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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“…Hierarchical clustering with the average linkage method was then used for the analysis of array CGH data (Snijders et al, 2005). To overcome scaling problems, we used the Spearman rank correlation distance, as it is scale independent (Eisen et al, 1998).…”

Section: Meta-analysis Proceduresmentioning

confidence: 99%

Cross-platform array comparative genomic hybridization meta-analysis separates hematopoietic and mesenchymal from epithelial tumors

et al. 2006

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A series of studies have been published that evaluate the chromosomal copy number changes of different tumor classes using array comparative genomic hybridization (array CGH); however, the chromosomal aberrations that distinguish the different tumor classes have not been fully characterized. Therefore, we performed a meta-analysis of different array CGH data sets in an attempt to classify samples tested across different platforms. As opposed to RNA expression, a common reference is used in dual channel CGH arrays: normal human DNA, theoretically facilitating cross-platform analysis. To this aim, cell line and primary cancer data sets from three different dual channel array CGH platforms obtained by four different institutes were integrated. The cell line data were used to develop preprocessing methods, which performed noise reduction and transformed samples into a common format. The transformed array CGH profiles allowed perfect clustering by cell line, but importantly not by platform or institute. The same preprocessing procedures used for the cell line data were applied to data from 373 primary tumors profiled by array CGH, including controls. Results indicated that there is no apparent feature related to the institute or platform and that array CGH allows for unambiguous cross-platform meta-analysis. Major clusters with common tissue origin were identified. Interestingly, tumors of hematopoietic and mesenchymal origins cluster separately from tumors of epithelial origin. Therefore, it can be concluded that chromosomal aberrations of tumors from hematopoietic and mesenchymal origin versus tumors of epithelial origin are distinct, and these differences can be picked up by meta-analysis of array CGH data. This suggests the possibility of prospectively using combined analysis of diverse copy number data sets for cancer subtype classification.

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Rare amplicons implicate frequent deregulation of cell fate specification pathways in oral squamous cell carcinoma

Cited by 245 publications

References 48 publications

Identification of differentially expressed genes in clear cell renal cell carcinoma by analysis of full-length enriched cDNA library

Identification of differentially expressed genes in clear cell renal cell carcinoma by analysis of full-length enriched cDNA library

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

Cross-platform array comparative genomic hybridization meta-analysis separates hematopoietic and mesenchymal from epithelial tumors

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