Myxoid liposarcoma tumor gene expression by array analysis
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ABSTRACT:
PROVIDER: PRJNA704029 | ENA |
REPOSITORIES: ENA
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Project description:Gene expression analysis of myxoid liposarcoma (MLS) tumors from five different patients
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Project description:In order to identify new key molecules in the pathogenesis of myxoid liposarcoma, we performed comparative gene expression profiling in myxoid liposarcoma and fat tissue samples.
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Project description:In order to identify new key molecules in the pathogenesis of myxoid liposarcoma, we performed comparative gene expression profiling in myxoid liposarcoma and fat tissue samples. Whole genome microarray analysis was performed on eight primary myxoid liposarcoma samples and an RNA pool of eight healthy fat tissue samples.
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Project description:miR-135b expression is higher in myxoid liposarcoma cell lines than in adipose-derived mesenchymal cell line, as well as in myxoid liposarcoma tumors than in adjacent normal prostate tissues.To further investigate the molecular mechanisms regulated by miR-135b, we performed mRNA microarray analysis of cell cultures from myxoid liposarcoma cell line after transfections with miR-135b mimic or negative control.
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Project description:Round cell component is a resk factor associated with metastasis and poor prognosis in myxoid liposarcoma. To identify microRNAs which play a role in the malignancy of round cell component, we performed microRNA microarray analysis and compared the miRNA expression profilings between myxoid and round cell component.
2017-02-09 | GSE73348 | GEO
Project description:To identify molecular biomakers that are useful for diagnosis and its targeting treatment, we compared the gene expression profile of myxiod liposarcoma with that of normal fat tissue. In the present study, we studied about gene expression profiles comparing 6 non-preoperative myxoid liposarcoma with 3 normal fat tissue.
2015-08-01 | E-GEOD-59568 | biostudies-arrayexpress
Project description:Myxoid liposarcoma (MLS) is the second most common type of liposarcoma and is characterized by the fusion oncogene FUS‐DDIT3 or the less common EWSR1‐DDIT3. While the presence of FUS-DDIT3 as a driver oncoprotein in most MLS cases has been confirmed, the exact molecular action behind the capacity of FUS-DDIT3 for transformation is still unclear and therefore creates a challenge in finding new treatments against this type of cancer. The importance of the microenvironment for tumor progression have long been accepted and might also influence the effect of the fusion oncoprotein. However, due to a lack of relevant experimental model systems, it has been challenging to examine the microenvironmental impact in myxoid liposarcoma development. Therefore, we have developed a new model system utilizing scaffolds derived from myxoid liposarcoma patient-derived xenograft tumors that are decellularized and then repopulated with sarcoma cell lines. This cell culture system mimics in vivo-like tumor cell growth conditions and induce transcriptional changes within the cells. In order to investigate the effect of the microenvironment as well as the fusion oncogene, we analyzed myxoid liposarcoma cell lines as well as fibrosarcoma cells with and without ectopic FUS-DDIT3 expression cultured in scaffolds and adherent two-dimensional growth conditions. We identified several gene networks and processes that are uniquely associated with FUS-DDIT3 expression and with the microenvironment, respectively. The development of patient-derived scaffolds opens up new possibilities to understand tumor development.
2023-12-31 | GSE191132 | GEO
Project description:To identify potential SOX11 target genes in myxoid liposarcoma (MLS) we stably transfected codon optimized full-length human SOX11 into the SOX11 negative MLS cell line MLS-1765. An emtpy vector (EV) was used as control. Potential SOX11 target genes were correlated with data set GSE52390.
2017-01-31 | GSE85231 | GEO
Project description:Myxoid liposarcoma (MLS) is the second most common type of liposarcoma and is characterized by the fusion oncogene FUS‐DDIT3 or the less common EWSR1‐DDIT3. FUS-DDIT3 is causative in tumor development, but the molecular function of FUS-DDIT3 remains largely unknown. In addition, the tumor microenvironment is important in MLS development. However, due to a lack of relevant experimental model systems, it has been challenging to examine the microenvironmental impact in MLS development. Therefore, we have developed an in vivo-like experimental model system utilizing cell-free scaffolds derived from myxoid liposarcoma patient-derived xenograft tumors that can be repopulated with tumor cells. To study the effect of FUS-DDIT3 expression in combination with the MLS microenvironment, we analyzed MLS cell lines as well as fibrosarcoma cells with and without ectopic FUS-DDIT3 expression cultured in scaffolds using cells cultured in monolayers as reference. We identified several gene networks and processes that are uniquely associated with FUS-DDIT3 expression as well as microenvironment. The use of in vivo-like experimental systems opens new possibilities to understand tumor development and develop treatments.
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Project description:FUS-CHOP and EWS-CHOP balanced translocations characterize myxoid liposarcoma which encompasses myxoid (ML) and round cell (RC) variants initially believed to be distinct diseases. Currently, myxoid and RC liposarcoma are regarded to represent the well differentiated and the poorly differentiated ends, respectively, within spectrum of myxoid liposarcoma where the fusion proteins blocking lipogenic differentiation play a role in tumor initiation while molecular determinants associated to progression to RC remain poorly understood. Activation of AKT pathway sustained by PIK3CA and PTEN mutations and growth factor receptor signalling such as RET and IGF1R have been recently correlated with the increasing of aggressiveness and RC. Aim of the present study is to elucidate molecular events involved in driving round cell progression analyzing two small series of MLS selected to be representative of the two end of the gamut: the pure myxoid (0% of RC component) and RC with high cellular component (≥80%).
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