ACGH was used to identify the overall genomic imbalances of SCC of the vulva in 14 patients
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE38229 | GEO | 2013/01/16
SECONDARY ACCESSION(S): PRJNA167468
REPOSITORIES: GEO
Similar Datasets
Project description:The imbalances scored by arrayCGH mapped to different chromosomes with losses being more common than gains. Frequent losses of large chromosomal segments were scored from 3p and 8p whereas same-sized gains were frequent from 3q and 8q. This is the first study of vulvar tumors using arrayCGH, and some frequent imbalances could be defined precisely. 14 patients we analyzed without replicates against a commercial common reference.
2013-01-16 | E-GEOD-38229 | biostudies-arrayexpress
Project description:The genome of 14 vulvar SCC was analyzed by aCGH and microarray to identify common imbalances present in the tumors as well as which genes were deregulated. Overall there was a good concordance between the imbalances scored by aCGH and the level of gene expression found by microarray, i.e., the genes located in gained regions were overexpressed while those located in lost regions were found down-regulated.
2013-01-16 | GSE38228 | GEO
Project description:The genome of 14 vulvar SCC was analyzed by aCGH and microarray to identify common imbalances present in the tumors as well as which genes were deregulated. Overall there was a good concordance between the imbalances scored by aCGH and the level of gene expression found by microarray, i.e., the genes located in gained regions were overexpressed while those located in lost regions were found down-regulated. The whole-gene expression profile of 14 SCC of the vulva was compared to 5 normal vulvar samples to identify genes that were deregulated in the tumors genome. Vulvar hyperplasia 03-48 not further analyzed and not included in the normalized data but included in the non-normalized data
2013-01-16 | E-GEOD-38228 | biostudies-arrayexpress
Project description:To prospectively identify new oncogenes implicated in lung Squamous Cell Carcinoma pathogenesis, we investigated chromosome 3 aberrations in advanced tumours using arrayCGH. These aberrations are indeed among the most frequent aberrations in lung SCC and correlate with SCC patient's poor prognosis. We precisely map regions of recurrent losses at 3p and gains at 3q25-qter in a series of lung SCC. We moreover uncover 3q26.3-q27 high level amplifications in 20% of tumours. Keywords: ArrayCGH, Lung Squamous Cell Carcinoma, 3q26.3, SOX2
2010-02-10 | GSE14859 | GEO
Project description:To prospectively identify new oncogenes implicated in lung Squamous Cell Carcinoma pathogenesis, we investigated chromosome 3 aberrations in advanced tumours using arrayCGH. Chromosome 3 aberrations are indeed among the most frequent alterations in lung SCC and correlate with SCC patient's poor prognosis. We have precisely mapped regions of recurrent losses at 3p and gains at 3q25-qter in a series of lung SCC (GSE14859) amd moreover uncover 3q26.3-q27 high level amplifications in 20% of tumours. These amplicons were precisely mapped in these tumors using arraCGH with a 3q26.3 dedicated tiling array. Keywords : ArrayCGH, lung Squamous Cell Carcinoma, 3q26.3, SOX2 Keywords: ArrayCGH
2010-02-10 | GSE15079 | GEO
Project description:Marginal zone B-cell lymphomas (MZL) have been divided into three distinct subtypes (extranodal MZL of MALT type, nodal MZL; splenic MZL). Nevertheless, the relationship between them is still unclear. We performed a comprehensive analysis of genomic DNA copy number changes in a very large series of MZL cases with the aim of addressing this question. Samples from 218 MZL patients (25 nodal, 57 MALT, 134 splenic and two not better specified MZL) were analyzed with the Affymetrix Human Mapping 250K SNP arrays, and the data combined with matched gene expression in 33/218 cases. MALT lymphoma presented significantly more frequently gains at 3p, 6p, 18p and del(6q23) (TNFAIP3/A20), whilst splenic MZL was associated with del(7q31), del(8p). Nodal MZL did not show statistically significant differences when compared with MALT lymphoma while lacked the splenic MZL-related 7q losses. Gains of 3q and 18q gains were common to all three subtypes. Del(8p) was often present together with del(17p) (TP53). While del(17p) did not determine a worse outcome and del(8p) was only of borderline significance, the presence of both deletions had a highly significant negative impact on the outcome of splenic MZL.
2011-02-01 | GSE24881 | GEO
Project description:Marginal zone B-cell lymphomas (MZL) have been divided into three distinct subtypes (extranodal MZL of MALT type, nodal MZL; splenic MZL). Nevertheless, the relationship between them is still unclear. We performed a comprehensive analysis of genomic DNA copy number changes in a very large series of MZL cases with the aim of addressing this question. Samples from 218 MZL patients (25 nodal, 57 MALT, 134 splenic and two not better specified MZL) were analyzed with the Affymetrix Human Mapping 250K SNP arrays, and the data combined with matched gene expression in 33/218 cases. MALT lymphoma presented significantly more frequently gains at 3p, 6p, 18p and del(6q23) (TNFAIP3/A20), whilst splenic MZL was associated with del(7q31), del(8p). Nodal MZL did not show statistically significant differences when compared with MALT lymphoma while lacked the splenic MZL-related 7q losses. Gains of 3q and 18q gains were common to all three subtypes. Del(8p) was often present together with del(17p) (TP53). While del(17p) did not determine a worse outcome and del(8p) was only of borderline significance, the presence of both deletions had a highly significant negative impact on the outcome of splenic MZL. Copy number analysis of Affymetrix 250K Nsp SNP arrays was performed for a total of 218 MZL samples were analyzed by high resolution genome wide-DNA profiling: 57 MALT lymphoma, 134 splenic MZL, 25 nodal MZL and two MZL where allocation to a specific category was not possible.
2011-02-01 | E-GEOD-24881 | biostudies-arrayexpress
Project description:To prospectively identify new oncogenes implicated in lung Squamous Cell Carcinoma pathogenesis, we investigated chromosome 3 aberrations in advanced tumours using arrayCGH. These aberrations are indeed among the most frequent aberrations in lung SCC and correlate with SCC patient's poor prognosis. We precisely map regions of recurrent losses at 3p and gains at 3q25-qter in a series of lung SCC. We moreover uncover 3q26.3-q27 high level amplifications in 20% of tumours. Keywords: ArrayCGH, Lung Squamous Cell Carcinoma, 3q26.3, SOX2 Profiling of 26 advanced (stage III) lung SCC. Replicates : each tumor sample is hybridized together with a normal dna sample to one microarray. Each microarray contain 3 replicates per BAC clone.
2010-05-14 | E-GEOD-14859 | biostudies-arrayexpress
Project description:To prospectively identify new oncogenes implicated in lung Squamous Cell Carcinoma pathogenesis, we investigated chromosome 3 aberrations in advanced tumours using arrayCGH. Chromosome 3 aberrations are indeed among the most frequent alterations in lung SCC and correlate with SCC patient's poor prognosis. We have precisely mapped regions of recurrent losses at 3p and gains at 3q25-qter in a series of lung SCC (GSE14859) amd moreover uncover 3q26.3-q27 high level amplifications in 20% of tumours. These amplicons were precisely mapped in these tumors using arraCGH with a 3q26.3 dedicated tiling array. Keywords : ArrayCGH, lung Squamous Cell Carcinoma, 3q26.3, SOX2 Keywords: ArrayCGH Profiling of 5 advanced (stage III) lung SCC using a chromosome 3 array providing 3q26.3-q27 tiling coverage. Replicates : each array contains three replicates per clone and each sample is hybridized to two arrays, results are subsequently averaged.
2010-02-09 | E-GEOD-15079 | biostudies-arrayexpress
Project description:Post-transplant lymphoproliferative disorders (PTLD) are a major complication of solid organ transplantation and represent a cause of severe morbidity and mortality among transplanted patients. Apart from EBV infection, knowledge of the pathogenesis of monoclonal PTLD is limited. Powerful analysis techniques, such as whole genomic DNA profiling (arrayCGH), can improve our understanding of PTLD pathogenesis. Toward this aim, we obtained the whole genome profiling using the Affymetrix GeneChip Human Mapping 10k 2.0 from 20 cases of PTLD and we compared them with those assessed in 25 cases of DLBCL from immunocompetent patients, as a control group. Recurrent lesions were detected among all the samples. Chromosome 18q, 7q, 3q and 12 were the most common gains in DLBCL of immunocompetent hosts. Chromosomes 5p and 11p were commonly gained in PTLD-DLBCL. The latter had frequent losses of 6q, 17p, 1p, and 9p. Chromosome 12p was the most frequent target of deletions among PTLD-DLBCL. The LOH pattern was characterized by involvement of chromosomes 13q and 17p in DLBCL and 10, 1q, 9p and 11q among PTLD-DLBCL. Interestingly, LOH did not always match the DNA loss. In particular, chromosome 10 seemes to be targeted by uniparental disomy in PTLD. Small deletions and gains, involving both known (BCL2 and PAX5) and unknown genes (ZDHHC14), have been identified. Our data suggest that PTLD share, at a lower frequency, common genetic aberrations with DLBCL from immunocompetent patients. The demonstration of 9p13 amplification indicates the importance of PAX5 in PTLD. The combination of DNA copy number and LOH assessment lead to the hypothesis that uniparental disomy may be a potential mechanism in B-cell lymphomagenesis. Twenty specimens of monoclonal B-cell PTLD, collected from 20 solid organ transplant recipients. Experiment Overall Design: 20 PTLD samples. No technical replications. Experiment Overall Design: 25 DLBCL samples (20 patient + 5 cell lines). No technical replications.
2008-06-16 | E-GEOD-8123 | biostudies-arrayexpress