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Profiling DNA copy number alterations of myxofibrosarcomas with NimbleGen array CGH chips

ABSTRACT: Characterized by a wide histological spectrum, myxofibrosarcoma ranges from deceptively bland-appearing lesions to frankly pleomorphic sarcomas, representing a suitable model to elucidate the molecular aberrations in multistep disease progression. To explore cancer-associated genes of myxofibrosarcoma, ultrahigh-resolution array comparative genomic hybridization (aCGH) was used to profile DNA copy number alterations in myxofibrosarcoma tumor samples and cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE35483 | GEO | 2012/02/02

SECONDARY ACCESSION(S): PRJNA152373

REPOSITORIES: GEO

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Profiling DNA copy number alterations of myxofibrosarcomas with NimbleGen array CGH chips

Project description:Characterized by a wide histological spectrum, myxofibrosarcoma ranges from deceptively bland-appearing lesions to frankly pleomorphic sarcomas, representing a suitable model to elucidate the molecular aberrations in multistep disease progression. To explore cancer-associated genes of myxofibrosarcoma, ultrahigh-resolution array comparative genomic hybridization (aCGH) was used to profile DNA copy number alterations in myxofibrosarcoma tumor samples and cell lines. Along with normal reference DNA, 12 tumor samples and 2 cell lines (NMFH-1, OH931) of human myxofibrosarcoma were extracted for genomic DNAs, which were subjected to manufacturer’s (NimbleGen Inc) outsourcing service of DNA labeling, hybridization, and normalization of data obtained from 385K oligonucleotide array CGH chips.

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Project description:Soft tissue sarcomas are aggressive mesenchymal cancers that affect more than 10,600 new patients per year in the US, about 40% of whom will die of their disease. Soft tissue sarcomas exhibit remarkable histologic diversity, with more than 50 recognized subtypes, but our knowledge of their genomic alterations is limited. Here we describe the results of an integrative analysis of DNA sequence, copy number, and mRNA expression in 207 samples encompassing seven major subtypes. Genes mutated in more than 5% of samples within a subtype were KIT (in gastrointestinal stromal cell tumors, or GISTs), TP53 (pleomorphic liposarcomas), PIK3CA (myxoid/round-cell liposarcoma), and NF1 (both myxofibrosarcoma and pleomorphic liposarcoma). We show evidence that PIK3CA mutations, found in 18% of myxoid/round-cell liposarcomas, activate AKT in vivo and are associated with poor outcomes. Point mutations in the tumor suppressor gene NF1 were discovered in both myxofibrosarcomas and pleomorphic liposarcomas, while genomic deletions were observed in all subtypes at varying frequencies. Finally, we found that short hairpin RNA-based knockdown of a subset of genes that are amplified in dedifferentiated liposarcoma, including CDK4 and YEATS4, decreased cell proliferation. Our study yields the most detailed map of molecular alterations across diverse sarcoma subtypes to date and provides potential subtype-specific targets for therapy. Human soft-tissue sarcoma specimens were profiled on Affymetrix U133A arrays per manufacturer's instructions.

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Project description:We used array-based comparative genomic hybridization to identify copy number alterations in the TP53 and RB1 tumor suppressor genes in 64 myxofibrosarcoma and 30 undifferentiated pleomorphic sarcoma primary untreated tumor samples, and found that 68% of tumor samples had shallow or deep deletions in one or both genes.

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