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Gene amplification of the transcription factor DP1 and the CTNND1 in human lung cancer

ABSTRACT: The search for novel oncogenes is important because these could be the target of future specific anticancer therapies. In the present work, we report the identification of novel amplified genes in lung cancer. In order to find out novel amplified genes in lung cancer, we aligned the gene expression data of 69 human lung tumors according to the position of transcripts in the human genome and searched for clusters of overexpressed genes. We found a cluster in chromosomes 13q34 and 11q12 with gene overexpression in four of these tumors. Then, we performed FISH analysis in these amplicons, which clearly evidenced the presence of high level copy number in these chromosomal regions. We performed SNP arrays-based in the tumors that carried gene amplification. The results clearly evidenced the presence of a high level copy number amplicon in these specimens.

ORGANISM(S): Homo sapiens

PROVIDER: GSE21168 | GEO | 2010/04/11

SECONDARY ACCESSION(S): PRJNA126625

REPOSITORIES: GEO

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Gene amplification of the transcription factor DP1 and the CTNND1 in human lung cancer

Project description:The search for novel oncogenes is important because these could be the target of future specific anticancer therapies. In the present work, we report the identification of novel amplified genes in lung cancer. In order to find out novel amplified genes in lung cancer, we aligned the gene expression data of 69 human lung tumors according to the position of transcripts in the human genome and searched for clusters of overexpressed genes. We found a cluster in chromosomes 13q34 and 11q12 with gene overexpression in four of these tumors. Then, we performed FISH analysis in these amplicons, which clearly evidenced the presence of high level copy number in these chromosomal regions. We performed SNP arrays-based in the tumors that carried gene amplification. The results clearly evidenced the presence of a high level copy number amplicon in these specimens. We determined the genomic copy number profile of four squamous cell carcinoma (SCC) tumours using a SNP array, the Illumina Infinium HumanOmni1-Quad BeadChip.

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Co-amplification at 8p and 11q in breast tumors and cell lines with 8p11q array Genomic Comparative Hybridization

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Project description:Chromosomal regions harboring tumor suppressors and oncogenes are often deleted or amplified. Array comparative genomic hybridization (CGH) detects segmental DNA copy number alterations in tumor DNA relative to a normal control. The recent development of a bacterial artificial chromosome (BAC) array, that spans the human genome in a tiling path manner with >32,000 clones, has facilitated whole genome profiling at an unprecedented resolution. Using this technology, we comprehensively describe and compare the genomes of 28 commonly used non-small cell lung carcinoma cell models, derived from 18 adenocarcinomas, 9 squamous cell carcinomas, and 1 large cell carcinoma. Analysis at such resolution not only provided a detailed genomic alteration template for each of these model cell lines, but revealed novel regions of frequent duplication and deletion. Significantly, a detailed analysis of chromosome 7 identified 6 distinct regions of alterations across this chromosome implicating the presence of multiple novel oncogene loci on this chromosome. As well, a comparison between the squamous and adenocarcinoma cells revealed alterations common to both subtypes, such as the loss of 3p and gain of 5p, in addition to multiple hotspots more frequently associated with only one subtype. Interestingly, chromosome 3q, which is known to be amplified in both subtypes, showed two distinct regions of alteration, one frequently altered in squamous and one more frequent altered in adenocarcinoma. In summary, our data demonstrates the unique information generated by high resolution analysis of NSCLC genomes and uncovers the presence of genetic alterations prevalent in the different NSCLC subtypes. Keywords: array CGH, amplification, segmental copy number, NSCLC, Lung cancer, genetic alterations

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Project description:Alterations in DNA copy number contribute to the development and progression of cancers and are common in epithelial tumors. We have used array Comparative Genomic Hybridization (aCGH) to visualize DNA copy number alterations across the genomes of lung tumors in the KrasLA2 model of lung cancer. Copy number gain involving the Kras locus, as focal amplification or whole chromosome gain, is the most common alteration in these tumors, and with a prevalence that increased significantly with increasing tumor size. Furthermore, Kras amplification was the only major genomic event among the smallest lung tumors, suggesting that this alteration occurs early during the development of mutant Kras driven lung cancers. Recurring gains and deletions of other chromosomes occur progressively more frequently among larger tumors. These results are in contrast to a previous aCGH analysis of lung tumors from KrasLA2 mice on a mixed genetic background, in which relatively few DNA copy alterations were observed regardless of tumor size. Our model features the KrasLA2 allele on the inbred FVB/N mouse strain, and in this genetic background there is a highly statistically significant increase in level of genomic instability with increasing tumor size. These data suggest that recurring DNA copy alterations are important for tumor progression in the KrasLA2 model of lung cancer, and that the requirement for these alterations may be dependent on the genetic background of the mouse strain.

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Affymetrix SNP array data for 47 lung squamous cell carcinoma and 40 esophageal squamous cell carcinoma samples.

Project description:Lineage-survival oncogenes are targeted by gene amplification in cancers arising from the tissues where these genes play a role in normal development. Here we show that the transcription factor SOX2—previously known to be mutated in hereditary human esophageal malformations, to be necessary for normal esophageal squamous development, to promote proliferation of basal tracheal cells and to co-operate in induction of pluripotent stem cells -- acts as an amplified oncogene in squamous cell carcinomas (SCC) of the lung and esophagus. We identified SOX2 at a peak of genomic amplification on chromosome 3q26.33 in SCCs of both the lung and esophagus but did not find it to be significantly amplified in adenocarcinomas from these tissues. Tumors with SOX2 amplification showed higher SOX2 mRNA expression, and suppression of SOX2 by RNAi in lung and esophageal SCC cell lines revealed that SOX2 expression is required for proliferation and anchorage-independent growth. Furthermore, ectopic expression of SOX2 cooperated with FOXE1 or FGFR2 to transform immortalized tracheobronchial epithelial cells. SOX2-driven tumors showed expression of markers of both squamous differentiation and pluripotency. These observations identify SOX2 as a novel lineage survival oncogene in lung and esophageal SCC and suggest novel connections between development, pluripotency and carcinogenesis.

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