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Gene Copy Number Aberrations are Associated with Survival in Histological Subgroups of Non-Small Cell Lung Cancer (expression data)

ABSTRACT: Hypothesis: Non-small cell lung cancer (NSCLC) is characterized by a multitude of genetic aberrations with unknown clinical impact. In this study, we aimed to identify gene copy number changes that correlate with clinical outcome in NSCLC. To maximize the chance to identify clinically relevant events, we applied a strategy involving two prognostically extreme patient groups. Results: Genetic aberrations were strongly associated with tumor histology. In adenocarcinoma (n=50), gene copy number gains on chromosome 8q21-q24.3 (177 genes) were more frequent in long-term survivors. In squamous cell carcinoma (n=28), gains on chromosome 14q23.1-24.3 (133 genes) were associated with shorter survival, whereas losses in a neighboring region, 14q31.1-32.33 (110 genes), correlated with favorable outcome. In accordance with copy number gains and losses, mRNA expression levels of corresponding genes were increased or decreased, respectively. Conclusion: Comprehensive tumor profiling permits the integration of genomic, histologic and clinical data. We identified gene copy number gains and losses, with corresponding changes in mRNA levels, that were associated with prognosis in adenocarcinoma and squamous cell carcinoma of the lung.

ORGANISM(S): Homo sapiens

PROVIDER: GSE28571 | GEO | 2011/10/28

SECONDARY ACCESSION(S): PRJNA143017

REPOSITORIES: GEO

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Gene Copy Number Aberrations are Associated with Survival in Histological Subgroups of Non-Small Cell Lung Cancer (copy number data)

Project description:Hypothesis: Non-small cell lung cancer (NSCLC) is characterized by a multitude of genetic aberrations with unknown clinical impact. In this study, we aimed to identify gene copy number changes that correlate with clinical outcome in NSCLC. To maximize the chance to identify clinically relevant events, we applied a strategy involving two prognostically extreme patient groups. Results: Genetic aberrations were strongly associated with tumor histology. In adenocarcinoma (n=50), gene copy number gains on chromosome 8q21-q24.3 (177 genes) were more frequent in long-term survivors. In squamous cell carcinoma (n=28), gains on chromosome 14q23.1-24.3 (133 genes) were associated with shorter survival, whereas losses in a neighboring region, 14q31.1-32.33 (110 genes), correlated with favorable outcome. In accordance with copy number gains and losses, mRNA expression levels of corresponding genes were increased or decreased, respectively. Conclusion: Comprehensive tumor profiling permits the integration of genomic, histologic and clinical data. We identified gene copy number gains and losses, with corresponding changes in mRNA levels, that were associated with prognosis in adenocarcinoma and squamous cell carcinoma of the lung.

2011-11-01 | GSE28572 | GEO

Gene Copy Number Aberrations are Associated with Survival in Histological Subgroups of Non-Small Cell Lung Cancer (copy number data)

2011-11-01 | E-GEOD-28572 | biostudies-arrayexpress

Gene Copy Number Aberrations are Associated with Survival in Histological Subgroups of Non-Small Cell Lung Cancer (expression data)

2011-10-27 | E-GEOD-28571 | biostudies-arrayexpress

Small bowel adenocarcinoma copy number profiles are more closely related to colorectal than to gastric cancers

Project description:Purpose: Small bowel adenocarcinoma (SBA) is a rare cancer and consequently the number of clinical trials has been very limited due to the small numbers of patients. Chemotherapy regimens are currently rather arbitrarily chosen between either a colorectal (CRC) or a gastric cancer (GC) regimen. Chromosomal copy number aberrations are a hallmark of solid tumours and can be measured by array comparative genomic hybridization (aCGH). The aim of the present study is to investigate whether genome-wide copy number aberrations of SBA are more similar to CRC or GC in order to support treatment of SBA according to either regimen. Experimental Design: A total of 85 GCs, CRCs and SBAs were selected from existing in house aCGH datasets based on array quality and clinical parameters. Differences and similarities in gains and losses of the three tumor types were analyzed using supervised and unsupervised analysis. Results: Hierarchical clustering revealed substantial overlap of chromosomal copy number profiles between SBA and CRC and less overlap between SBA and GC. Chromosome 13q13.2-q31.3 is primarily gained in SBA and CRC and the strongest feature discriminating SBA from GC. Further strong discriminating copy number characteristics are aberrations at chromosomes 1p36.3-p34.3, 4p15.3-q35.2, 9p24.3-p11.1 and 17p13.3-p13.2. Conclusions: SBA is more similar to CRC than to GC, based on genome-wide copy number aberrations. These data provide molecular support for treatment of SBA according to a CRC regimen.

2011-06-13 | GSE23418 | GEO

Copy number alterations in 8 lung cancer in Xuanwei samples

Project description:In order to screen potential novel 'driver genes' in lung cancer in Xuanwei (LCXW), genome-wide DNA copy number alterations (CNAs) were detected on 8 paired LCXW and non-cancerous lung (NCL) tissues by array-based comparative genomic hybridization microarrays. The log2 copy-number ratio calculation and CNA calls were determined using segMNT algorithm in NimbleScan. Log2 ratio test/control thresholds of 0.25 and -0.25 were defined as copy number gains and losses, respectively. Deviant signal intensity ratios involving 5 or more neighboring probes were considered as genomic aberrations. A large number of CNAs and DEGs were detected, respectively. Many recurrent CNAs were screened out, including gains at 5p15.33-p15.32, 5p15.1-p14.3 and 5p14.3-p14.2, and losses at 11q24.3, 21q21.1, 21q22.12-q22.13 and 21q22.2.

2016-10-22 | GSE89046 | GEO

Small bowel adenocarcinoma copy number profiles are more closely related to colorectal than to gastric cancers

2011-06-13 | E-GEOD-23418 | biostudies-arrayexpress

Affymetrix SNP 6.0 data for analysis of esophageal adenocarcinoma samples

Project description:Esophageal adenocarcinoma is characterized by complex chromosomal alterations. Tumors were evaluated to identify regions of recurrent copy gains and losses and to determine the prognositic significance of the degree of segmental aneuploidy as measured by SNP array. 41 superficial esophageal adenocarcinomas were analyzed for copy number abnormalities. Matched normal lymph node tissue was used as a copy number reference.

2013-12-01 | E-GEOD-49396 | biostudies-arrayexpress

Affymetrix SNP array data for NSCLC samples

Project description:Non-small cell lung cancer (NSCLC) presents a notoriously genomically unstable cancer type, with numerous large scale and focal genomic aberrations resulting in gene copy number variations across the whole genome. The relations of these gene copy number changes to subsequent mRNA levels are only fragmentarily understood. The aim of this study was an integrated analysis of gene copy number changes and corresponding gene expression in a large clinically annotated NSCLC patient cohort. Fresh frozen tumor sample from 190 resected NSCLC patients were subjected to SNP arrays and gene expression array analysis resulting 39788 tested copy number/ RNA expression pairs. Correlation analysis using an externally centered correlation coefficient (ECCC) revealed that gene expression of 19058 genes was significantly influenced by gene copy number changes (FDR < 0.05). However, only 440 probe sets demonstrated high correlations (ECCC > 0.7) that were mostly due to few cases with high gene copy number gains. These gene copy number dependent genes were clustered in only few chromosomal hot spot regions and classical oncogenes (e.g. EGFR, MDM2, KRAS) are overrepresented among these genes. In a meta-analysis, including 1585 NSCLC patients, gene expression levels from 70 of 440 (16%) gene-copy-number-dependent genes were associated with survival. In conclusion, the genome-wide analysis indicates that gene copy number aberrations influence directly gene expression levels in a distinct subset of genes. The concrete illustration of these molecular relations help to interpret the impact of gene copy number changes and may serve as starting points to identify new cancer drivers in NSCLC.

2016-08-31 | GSE76730 | GEO

Predicting drug activity in non-small cell lung cancer based on genetic lesions

Project description:84 NSCLC cell lines were collected from various sources (Supplemental Table 1) and formed the basis for all subsequent experiments. Cell lines were derived from tumors representing all major subtypes of NSCLC tumors, including adenocarcinoma, squamous-cell carcinoma and large-cell carcinoma. The genomic landscape of these cell lines was characterized by analyzing gene copy number alterations using high-resolution single-nucleotide polymorphism (SNP) arrays (250K Sty1). We used the statistical algorithm Genomic Identification of Significant Targets in Cancer (GISTIC) to distinguish biologically relevant lesions from background noise. The application of GISTIC revealed 16 regions of recurrent, high-level copy number gain (inferred copy number > 2.14) and 20 regions of recurrent copy number loss (inferred copy number < 1.86)

2009-07-29 | GSE17247 | GEO

Affymetrix SNP array data for 30 NSCLC samples

Project description:In cancer, proto-oncogenes are often altered by genomic amplification. Recent studies have highlighted a role for PDGFRA as an oncogene in non-small cell lung cancer. To characterize 4q12 copy number status in NSCLC, both previously published (Weir et al. PMID 17982442) and unpublished Affymetrix 250K SNP array data for 733 NSCLC samples (628 primary samples, 105 cell lines) were evaluated for copy number aberrations. 4q12 amplifications overlapping the PDGFRA/KIT locus were observed in 31 (4.2%) NSCLC samples. SNP array and FISH analysis indicate that 4q12 is amplified in 3-7% of lung adenocarcinomas and 8-10% of lung squamous cell carcinomas. In addition, the NSCLC cell line NCI-H1703 exhibits focal amplification of PDGFRA and is dependent on PDGFRα activity for cell growth. Treatment of NCI-H1703 cells with PDGFRA-specific shRNAs or with the PDGFRα/KIT small molecule inhibitors imatinib or sunitinib leads to cell growth inhibition. However, these observations do not extend to NSCLC cell lines with lower-amplitude and broader gains of chromosome 4q. Together these observations implicate PDGFRA and KIT as potential oncogenes in NSCLC, but further study is needed to define the specific characteristics of those tumors that could respond to PDGFRα/KIT inhibitors.

2009-09-15 | GSE17429 | GEO

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