Genomic copy number aberrations in primary lung squamous cell carcinoma
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE43131 | GEO | 2015/09/22
SECONDARY ACCESSION(S): PRJNA184677
REPOSITORIES: GEO
Similar Datasets
Project description:Chromosomal instability is one of the hallmarks of tumors, which can result in the gain or loss of specific genomic regions or even entire chromosomes. These copy number aberrations (CNAs) play an important role in carcinogenesis and malignant progression through CNA-induced gene expression alterations and, subsequently, key cancer-specific processes. In the current study, we applied aCGH analysis to screen out CNAs with potential prognostic value in lung SCC patients. Depending on their survival time, 100 patients with primary SCC were separated into high- or low-risk groups of prognosis, and copy number aberration (CNA) were analyzed by array-comparative genomic hybridization (array-CGH).
2015-09-22 | E-GEOD-43131 | biostudies-arrayexpress
Project description:Cancer is a genetic disease with frequent somatic alterations in DNA. Study of recurrent copy number aberrations (CNAs) in human cancers would enable the elucidation of disease mechanisms and the identification of key oncogenic drivers with causal roles in oncogenesis. We have comprehensively and systematically characterized CNAs and accompanied gene expression changes in the tumors and their matched non-tumor liver tissues from 286 hepatocellular carcinoma (HCC) patients. Our analysis identified 29 recurrently amplified regions and 22 deleted regions with a high level of copy number changes, harboring established oncogenes and tumor suppressors, including CCND1, MET, CDKN2A and CDKN2B, as well as many other genes not previously reported to be involved in liver carcinogenesis. Cis-acting genes in the amplification and deletion peaks were enriched in core cancer pathways, including cell cycle, p53, PI3K, MAPK, Wnt and TGFβ signaling in large proportions of HCCs. We further validated two candidate driver genes, BCL9 and MTDH, from the recurrent focal amplification peaks and showed that they play a significant role in HCC growth and survival. In summary, we have demonstrated that characterizing the CNA landscape in HCC will facilitate the understanding of disease mechanisms and the identification of oncogenic drivers that may serve as potential therapeutic targets for the treatment of this devastating disease.
2013-05-22 | GSE38323 | GEO
Project description:Cancer is a genetic disease with frequent somatic alterations in DNA. Study of recurrent copy number aberrations (CNAs) in human cancers would enable the elucidation of disease mechanisms and the identification of key oncogenic drivers with causal roles in oncogenesis. We have comprehensively and systematically characterized CNAs and accompanied gene expression changes in the tumors and their matched non-tumor liver tissues from 286 hepatocellular carcinoma (HCC) patients. Our analysis identified 29 recurrently amplified regions and 22 deleted regions with a high level of copy number changes, harboring established oncogenes and tumor suppressors, including CCND1, MET, CDKN2A and CDKN2B, as well as many other genes not previously reported to be involved in liver carcinogenesis. Cis-acting genes in the amplification and deletion peaks were enriched in core cancer pathways, including cell cycle, p53, PI3K, MAPK, Wnt and TGFβ signaling in large proportions of HCCs. We further validated two candidate driver genes, BCL9 and MTDH, from the recurrent focal amplification peaks and showed that they play a significant role in HCC growth and survival. In summary, we have demonstrated that characterizing the CNA landscape in HCC will facilitate the understanding of disease mechanisms and the identification of oncogenic drivers that may serve as potential therapeutic targets for the treatment of this devastating disease.
2013-05-22 | GSE38207 | GEO
Project description:Cancer is a genetic disease with frequent somatic alterations in DNA. Study of recurrent copy number aberrations (CNAs) in human cancers would enable the elucidation of disease mechanisms and the identification of key oncogenic drivers with causal roles in oncogenesis. We have comprehensively and systematically characterized CNAs and accompanied gene expression changes in the tumors and their matched non-tumor liver tissues from 286 hepatocellular carcinoma (HCC) patients. Our analysis identified 29 recurrently amplified regions and 22 deleted regions with a high level of copy number changes, harboring established oncogenes and tumor suppressors, including CCND1, MET, CDKN2A and CDKN2B, as well as many other genes not previously reported to be involved in liver carcinogenesis. Cis-acting genes in the amplification and deletion peaks were enriched in core cancer pathways, including cell cycle, p53, PI3K, MAPK, Wnt and TGFβ signaling in large proportions of HCCs. We further validated two candidate driver genes, BCL9 and MTDH, from the recurrent focal amplification peaks and showed that they play a significant role in HCC growth and survival. In summary, we have demonstrated that characterizing the CNA landscape in HCC will facilitate the understanding of disease mechanisms and the identification of oncogenic drivers that may serve as potential therapeutic targets for the treatment of this devastating disease. Two hundred and eighty-six hepatocellular carcinoma tumors and their matched non-tumor adjacent liver tissue samples were genotyped using Illumina HumanOmni1-Quad BeadChip to estimate their somatic copy number profiles.
2013-05-22 | E-GEOD-38323 | biostudies-arrayexpress
Project description:Cancer is a genetic disease with frequent somatic alterations in DNA. Study of recurrent copy number aberrations (CNAs) in human cancers would enable the elucidation of disease mechanisms and the identification of key oncogenic drivers with causal roles in oncogenesis. We have comprehensively and systematically characterized CNAs and accompanied gene expression changes in the tumors and their matched non-tumor liver tissues from 286 hepatocellular carcinoma (HCC) patients. Our analysis identified 29 recurrently amplified regions and 22 deleted regions with a high level of copy number changes, harboring established oncogenes and tumor suppressors, including CCND1, MET, CDKN2A and CDKN2B, as well as many other genes not previously reported to be involved in liver carcinogenesis. Cis-acting genes in the amplification and deletion peaks were enriched in core cancer pathways, including cell cycle, p53, PI3K, MAPK, Wnt and TGFβ signaling in large proportions of HCCs. We further validated two candidate driver genes, BCL9 and MTDH, from the recurrent focal amplification peaks and showed that they play a significant role in HCC growth and survival. In summary, we have demonstrated that characterizing the CNA landscape in HCC will facilitate the understanding of disease mechanisms and the identification of oncogenic drivers that may serve as potential therapeutic targets for the treatment of this devastating disease. Thirty hepatocellular carcinoma cell lines were genotyped using Illumina HumanOmni1-Quad BeadChip to estimate their copy number profiles relative to pooled Hapmap samples.
2013-05-22 | E-GEOD-38207 | biostudies-arrayexpress
Project description:Large but not small copy-number alterations correlate to high-risk genomic aberrations and survival in chronic lymphocytic leukemia: a high-resolution genomic screening of newly diagnosed patients. Single nucleotide polymorphism (SNP)-arrays allow simultaneous detection of copy-number aberrations (CNAs) and copy-number neutral loss-of-heterozygosity (CNN-LOH). In this study we investigated the presence of CNAs and CNN-LOH in newly diagnosed CLL samples from a Swedish chronic lymphocytic leukemia (CLL) cohort. In this study we could detect the known recurrent aberrations in CLL (i.e. deletions of 13q, 11q, 17p and trisomy 12). We also detected other both large and small CNAs which were mostly non-recurrent. CNN-LOH was detected on chromosome 13q in patients that carried homozygous deletion of 13q.
2009-11-23 | GSE16406 | GEO
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
Project description:In the breast, the reduction of invasive ductal carcinoma (IDC) seems to be smaller than expected from an increasing number of ductal carcinoma in situ (DCIS) detection in screening programs, suggesting that some DCIS lesions remain dormant and take a very long time for progression to IDC. However, the progression risk of individual DCIS and papilloma to IDC largely remain unassessable. To tackle this problem, we applied array-based comparative genomic hybridization to DCIS, IDC and papilloma lesions. We confirmed the presence of chromosomal copy-number alterations (CNAs) reported previously in breast cancers and the absence of chromosomal CNAs in the papillomas examined. These findings suggest that gene CNA profile is a good lineage marker for prediction of progression risk of individual tumors and that tumor progression within each lineage is driven by epigenetic rather than genetic alterations.
2016-09-16 | GSE86988 | GEO
Project description:Characterization of chromosomal aberrations in liver tumors of Tak1-/- mice of different ages The aim of the project is to dissect signaling mechanisms which could be of importance during the process of liver carcinogenesis. Keywords: Array comparative genomic hybridization analysis (aCGH).
2010-03-31 | GSE19105 | GEO
Project description:Breast cancer is the most prevalent cancer in women 1, and most cases are believed to have a sporadic, rather than heritable basis 2. To identify breast cancer driver genes, we exploited the C3H-Mcm4Chaos3/Chaos3 (“Chaos3”) mouse model that, by virtue of bearing a defective DNA replicative helicase subunit that causes elevated genomic instability (GIN), sustains somatic alterations ultimately causing mammary adenocarcinomas 6. Array Comparative Genomic Hybridization (aCGH) analysis of Chaos3 mammary tumors revealed recurrent copy number alterations (CNAs), most notably deletion of the Neurofibromin 1 (Nf1) tumor suppressor gene in all cases. NF1, a negative regulator of RAS, is traditionally recognized for its role in driving the development of neurofibromas in the context of the human disease Neurofibromatosis Type 1, but not breast cancer. Genomic DNA from tumor and reference samples were hybridized to NimbleGen 3x720K mouse CGH arrays. Two reference samples were used independently. CNAs were visualized using Nimblegen, IGV, and KCsmart software 32. Select genes were validated via qPCR. Critical regions within each Chaos3 CNA were identified as the region with the greatest overlap across multiple Chaos3 tumors. Recurring Copy Number Variations (CNVs) for 12 Chaos3 tumors and 2 MMTV-Neu mammary tumors analyzed by aCGH are indicated. Samples analyzed are primary tumors except where indicated.
2012-10-01 | E-GEOD-37607 | biostudies-arrayexpress