Two genetic pathways in myxoinflammatory fibroblastic sarcoma and morphologically similar lesions
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE12595 | GEO | 2009/01/26
SECONDARY ACCESSION(S): PRJNA112845
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE12592: Gene expression analysis of myxoinflammatory fibroblastic sarcoma, and morphologically similar lesions GSE12593: DNA copy number analysis of myxoinflammatory fibroblastic sarcoma, and morphologically similar lesions Refer to individual Series
2009-01-25 | E-GEOD-12595 | biostudies-arrayexpress
Project description:Global gene expression analysis was performed in cases 1, 2, 5, 6 and 8 as well as in five pooled myxofibrosarcomas using the Affymetrix GeneChip Human Gene 1.0 ST Arrays (Affymetrix Inc., Santa Clara, CA, USA). Unsupervised hierarchical clustering analysis, using Pearson correlation and average linkage clustering, separated the control pool and case 6 from the rest of the cases. Cases 1 and 5, both harboring t(1;10)(p22;q24), were in turn segregated from cases 2 and 8. Tumors with t(1;10)(p22;q24) thus seemed to have a more distinct expression pattern than tumors affected by amplification of regions on chromosome 3. Tumors with t(1;10) showed increased expression levels of NPM3 and FGF8 compared with tumors without such a translocation, including the control pool. No other gene in the 5 Mb region proximal to the breakpoint on chromosome 10 displayed a more pronounced difference between the two groups. Of the genes located in the commonly amplified region on chromosome 3, VGLL3 and CHMP2B showed a higher expression in tumors affected by the amplification.
2009-01-26 | GSE12592 | GEO
Project description:DNA copy number analysis of myxoinflammatory fibroblastic sarcomas, and related lesions, using 32k BAC array CGH. All four cases analyzed with array CGH showed amplification of the region 86.30-87.74 Mb in 3p11.1-12.1. No additional aberration was detected in more than two tumors, except for the deletion distal to the amplification on chromosome 3. Case 1 showed deletion affecting the region from the centromere of chromosome 1 to the 5'-end of TGFBR3. Homozygous deletion was found in one case (case 6) affecting the region 21.08-22.15 Mb on chromosome arm 9p harboring the CDKN2A and CDKN2B genes.
2009-01-26 | GSE12593 | GEO
Project description:Global gene expression analysis was performed in cases 1, 2, 5, 6 and 8 as well as in five pooled myxofibrosarcomas using the Affymetrix GeneChip Human Gene 1.0 ST Arrays (Affymetrix Inc., Santa Clara, CA, USA). Unsupervised hierarchical clustering analysis, using Pearson correlation and average linkage clustering, separated the control pool and case 6 from the rest of the cases. Cases 1 and 5, both harboring t(1;10)(p22;q24), were in turn segregated from cases 2 and 8. Tumors with t(1;10)(p22;q24) thus seemed to have a more distinct expression pattern than tumors affected by amplification of regions on chromosome 3. Tumors with t(1;10) showed increased expression levels of NPM3 and FGF8 compared with tumors without such a translocation, including the control pool. No other gene in the 5 Mb region proximal to the breakpoint on chromosome 10 displayed a more pronounced difference between the two groups. Of the genes located in the commonly amplified region on chromosome 3, VGLL3 and CHMP2B showed a higher expression in tumors affected by the amplification. Cases 1, 2, 5, 6 and 8 were analyzed using the GeneChip Human Gene 1.0 ST Arrays (Affymetrix Inc, Santa Clara, CA, USA). As a control, a pool of five myxofibrosarcomas was used. Total RNA was extracted from frozen tumor biopsies using TRIzol reagent (Invitrogen, Carlsbad, CA, USA) and RNeasy (Qiagen, Valencia, CA, USA) according to the manufacturers’ instructions. RNA quality and concentration were measured using an Agilent 2100 bioanalyzer and Nanodrop ND-1000, respectively. cDNA was generated with the GeneChip® Whole Transcript (WT) cDNA Synthesis and Amplification Kit (Affymetrix) using 300 ng total RNA. Amplified cDNA was fragmented and end labeled using the GeneChip® WT Terminal Labelling Kit (Affymetrix). Subsequently, the fragmented and biotinylated cDNA was hybridized to the GeneChip® Human Gene 1.0 ST Arrays (Affymetrix). The arrays were washed and stained on a GeneChip® Fluidics Station 450 (Affymetrix) according to the manufacturer’s recommendations. Scanning was carried out with the GeneChip® Scanner 3000 and image analysis was performed using GeneChip® Operating Software (GCOS, Affymetrix). Expression data was normalized, background corrected and summarized using the RMA algorithm implemented in the Affymetrix Expression Console™ version 1.0 software. Clustering was performed with MeV 4.1.01 software (http://www.tm4.org/mev.html), using unsupervised hierarchical clustering analysis on the basis of Pearson correlation and average linkage clustering.
2009-01-25 | E-GEOD-12592 | biostudies-arrayexpress
Project description:DNA copy number analysis of myxoinflammatory fibroblastic sarcomas, and related lesions, using 32k BAC array CGH. All four cases analyzed with array CGH showed amplification of the region 86.30-87.74 Mb in 3p11.1-12.1. No additional aberration was detected in more than two tumors, except for the deletion distal to the amplification on chromosome 3. Case 1 showed deletion affecting the region from the centromere of chromosome 1 to the 5'-end of TGFBR3. Homozygous deletion was found in one case (case 6) affecting the region 21.08-22.15 Mb on chromosome arm 9p harboring the CDKN2A and CDKN2B genes. DNA copy numbers in cases 1 and 6-8 were analyzed using tiling microarrays containing more than 32 000 partly overlapping BAC clones, generating complete coverage of the human genome (Jönsson et al., 2007, Genes Chromosomes Cancer 46: 543-58.). The arrays were produced at the Swegene DNA Microarray Resource Center, Department of Oncology, Lund University (http://swegene.onk.lu.se), as previously described (Jönsson et al., 2007), using BAC clones mapped to the hg17 genome build. Extraction, labeling and hybridization of genomic DNA from freshly frozen tumor biopsies, as well as pretreatment and washing of slides were performed as described (Heidenblad et al., 2006, Oncogene 25: 7106-16). As a control for normal copy number, a DNA pool derived from multiple healthy male donors was used (Promega, Madison, WI, USA). Primary array CGH data were collected using the GenePix Pro 4.0 (Axon Instruments Inc., Foster City, CA, USA). The quantified data matrix was deposited into the web-based database BioArray Software Environment (BASE) (Saal et al., 2002, Genome Biol 3: software0003.1-0003.6), and data analyses were done as described (Hallor et al., 2008, Br J Cancer 98: 434-42). In brief, following background correction the log(2) ratios were calculated for each spot, and unreliable features and spots not showing signal-to-noise ratios ?5 for both channels were eliminated. Normalization of data was performed using pin-based Lowess normalization and single outlier probes were removed. Thereafter, the log(2) ratios for each sample were segmented, followed by elimination of segments less than 500 kb in size. Copy number alterations were determined by comparing the segmented log(2) ratios to gain/loss thresholds obtained by an adaptive scaling method (Staaf et al., 2007, BMC Genomics 8: 382).
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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
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