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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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ACGH data for mesothelioma cell lines

ABSTRACT: Malignant pleural mesotheliomas (MPMs) often show CDKN2A and NF2 inactivation but other highly recurrent mutations have not been described. To identify additional driver genes, we used an integrated genomic analysis of 53 MPM tumor samples to guide a focused sequencing effort that uncovered somatic inactivating mutations in BAP1 in 23% of MPM. The BAP1 nuclear deubiquitinase is known to target histones (together with ASXL1 as a Polycomb repressor subunit) and the HCF1 transcriptional co-factor, and we show that BAP1 knockdown in MPM cell lines affects E2F and Polycomb target genes. These findings implicate transcriptional deregulation in the pathogenesis of MPM. Genomic DNA was harvested from untreated malignant pleural mesothelioma (MPM) cell lines and used to generate gain/loss profiles for each line using aCGH.

ORGANISM(S): Homo sapiens

SUBMITTER: Yupu Liang

PROVIDER: E-GEOD-29383 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Mesothelioma tumor aCGH profiles

Project description:Malignant pleural mesotheliomas (MPMs) often show CDKN2A and NF2 inactivation but other highly recurrent mutations have not been described. To identify additional driver genes, we used an integrated genomic analysis of 53 MPM tumor samples to guide a focused sequencing effort that uncovered somatic inactivating mutations in BAP1 in 23% of MPM. The BAP1 nuclear deubiquitinase is known to target histones (together with ASXL1 as a Polycomb repressor subunit) and the HCF1 transcriptional co-factor, and we show that BAP1 knockdown in MPM cell lines affects E2F and Polycomb target genes. These findings implicate transcriptional deregulation in the pathogenesis of MPM. DNA from 53 malignant pleural mesothelioma tumors was collected and hybridized to aCGH arrays. Data were analyzed to create gain and loss profiles for each tumor. This submission includes gcNormalized-data.

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Project description:Malignant pleural mesotheliomas (MPMs) often show CDKN2A and NF2 inactivation but other highly recurrent mutations have not been described. To identify additional driver genes, we used an integrated genomic analysis of 53 MPM tumor samples to guide a focused sequencing effort that uncovered somatic inactivating mutations in BAP1 in 23% of MPM. The BAP1 nuclear deubiquitinase is known to target histones (together with ASXL1 as a Polycomb repressor subunit) and the HCF1 transcriptional co-factor, and we show that BAP1 knockdown in MPM cell lines affects E2F and Polycomb target genes. These findings implicate transcriptional deregulation in the pathogenesis of MPM. Total RNA from 53 pleural mesothelioma tumors was extracted and hybridized to Affymetrix gene expression arrays to compile a set of gene expression profiling data for this disease.

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