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Validation of dedifferentiated liposarcoma (DDLS) cell lines with the original tumors via copy number alteration analysis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE184702 | GEO | 2021/12/31

REPOSITORIES: GEO

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Validation of dedifferentiated liposarcoma (DDLS) cell lines with the original tumors via copy number alteration analysis [array]

Project description:We validated patient's tumor-derived cell lines of liposarcoma by analysing copy number alterations using aCGH or WGS and comparing with the original tumor tissues. examination of copy number alterations for 2 cell lines, one of the original tumor, one PDX-tumor and its original tumor.

2021-12-31 | GSE184701 | GEO

Validation of dedifferentiated liposarcoma (DDLS) cell lines with the original tumors via copy number alteration analysis [sequencing]

Project description:We validated patient's tumor-derived cell lines of liposarcoma by analysing copy number alterations using aCGH or WGS and comparing with the original tumor tissues.

2021-12-31 | GSE184700 | GEO

Validation of dedifferentiated liposarcoma (DDLS) cell lines with the original tumors via copy number alteration analysis

Project description:Validation of dedifferentiated liposarcoma (DDLS) cell lines with the original tumors via copy number alteration analysis

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Validation of dedifferentiated liposarcoma (DDLS) cell lines with the original tumors via copy number alteration analysis [sequencing]

Project description:Validation of dedifferentiated liposarcoma (DDLS) cell lines with the original tumors via copy number alteration analysis [sequencing]

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Validation of dedifferentiated liposarcoma (DDLS) cell lines with the original tumors via copy number alteration analysis [array]

Project description:Validation of dedifferentiated liposarcoma (DDLS) cell lines with the original tumors via copy number alteration analysis [array]

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Copy number losses define subgroups of dedifferentiated liposarcoma with poor prognosis and genomic instability.

Project description:Molecular events underlying progression of well-differentiated liposarcoma (WDLS) to dedifferentiated liposarcoma (DDLS) are poorly defined. This study sought to identify copy number alterations (CNA) associated with dedifferentiation of WDLS, with DDLS morphology, and with patient outcomes.Fifty-five WDLS and 52 DDLS were analyzed using Agilent 244K comparative genomic hybridization and Affymetrix U133A expression arrays. CNAs were identified by RAE analysis. Thirty-nine of the DDLS specimens were categorized morphologically by a single pathologist.Nine regions of CNA were identified as recurrent in DDLS but not WDLS; 79% of DDLS had at least one of these CNAs. Loss of the chromosome segment 11q23-24, the most common event, was observed only in DDLS that morphologically resembled the genomically complex sarcomas, undifferentiated pleomorphic sarcoma and myxofibrosarcoma. 11q23-24 loss was itself associated with increased genomic complexity in DDLS. Loss of 19q13, but not 11q23-24, was associated with poor prognosis. Median disease-specific survival was shorter for patients with19q13 loss (27 months) than for patients with diploid 19q13 (>90 months; P < 0.0025), and 19q13 loss was associated with local recurrence (HR, 2.86; P = 0.013). Common copy number losses were associated with transcriptional downregulation of potential tumor suppressors and adipogenesis-related genes (e.g., EI24 and CEBPA).Dedifferentiation of WDLS is associated with recurrent CNAs in 79% of tumors. In DDLS, loss of 11q23-24 is associated with genomic complexity and distinct morphology whereas loss of 19q13 predicts poor prognosis. CNAs in liposarcoma improve risk stratification for patients and will help identify potential tumor suppressors driving liposarcoma progression.

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Drug Synergy Screen and Network Modeling in Dedifferentiated Liposarcoma (DDLS)

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-09-24 | GSE50751 | GEO

Drug Synergy Screen and Network Modeling in Dedifferentiated Liposarcoma (DDLS)

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-09-24 | E-GEOD-50751 | biostudies-arrayexpress

Pathogenic NF1 truncating mutation and copy number alterations in a dedifferentiated liposarcoma with multiple lung metastasis: a case report.

Project description:BACKGROUND:Dedifferentiated liposarcoma (DDLPS), which accounts for an estimated 15-20% of liposarcomas, is a high-grade and aggressive malignant neoplasm, exhibiting a poor response to available therapeutic agents. However, genetic alteration profiles of DDLPS as well as the role of NF1 mutations have not been studied extensively. CASE PRESENTATION:The current study reports a patient presenting with rapidly growing DDLPS accompanied by multiple lung and pleural metastases, in whom whole-exome sequencing revealed a NF1 truncating mutation of the known pathogenic variant, c.C7486T, p.R2496X, as well as multiple copy number alterations (CNAs), including the well-known 12q13-15 amplification, and multiple chromothripsis events encompassing potential cancer-related genes. CONCLUSIONS:Our results suggest that, in addition to the 12q13-15 amplification, NF1 inactivation mutation and other CNAs may contribute to DDLPS tumorigenesis accompanied by aggressive clinical features.

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Association of FOSL1 copy number alteration and triple negative breast tumors.

Project description:Copy number alterations (CNAs) are a frequent feature in human breast cancer, and one of the hallmarks of genomic instability. The FOSL1, GSTP1 and CCND1 genes are located at 11q13, a cytoband commonly affected by CNA in breast cancer, with relevant function in progression and invasion. Our main goal was to analyze CNAs of these genes and determine their association with breast cancer subtypes. Seventy-three cases of invasive breast tumors [52 Luminal, 7 HER2+ and 14 triple negative (TNBC) subtypes] were analyzed by TaqMan assays. CNAs were observed for all genes, with gains more frequently observed. Gains of the FOSL1 gene were observed in 71% of the cases. This gene was the only one with a statistically significant difference (p<0.001) among tumor subtypes, with increased copy number in TNBC compared to luminal and HER2+. No significant association of CNA and clinical and histopathological parameters from the patients was observed. Additional studies in larger breast cancer patient cohorts based on more refined molecular subtypes are necessary to confirm the observed association of FOSL1 gain with aggressive breast tumors phenotypes.

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