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20 human soft-tissue sarcomas (TMT)

ABSTRACT: SCX fractiond, TMT labeled pleomorphic soft-tissue sarcomas. 32 raw files (8x4) plus 8 pools (also TMT labeled) corresponding to each SCX fraction are submitted. The latter were used to propagate identifications across the runs.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Soft Tissue Sarcoma Cell

SUBMITTER: Ufuk Kirik

LAB HEAD: Ana Carneiro

PROVIDER: PXD000617 | Pride | 2020-01-27

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	110921_LA_PoolASarcoma_SCX1_01.raw	Raw
	110921_LA_PoolASarcoma_SCX1_01_20110928_F007445.xml	Xml
	110921_LA_PoolASarcoma_SCX1_01_GPM00300017783.2011_09_28_16_49_12.t.xt.xml	Xml
	110921_LA_PoolASarcoma_SCX2_01.raw	Raw
	110921_LA_PoolASarcoma_SCX2_01_20110928_F007446.xml	Xml

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Publications

Discovery-based protein expression profiling identifies distinct subgroups and pathways in leiomyosarcomas.

Kirik Ufuk U Hansson Karin K Krogh Morten M Jönsson Mats M Nilbert Mef M James Peter P Carneiro Ana A

Molecular cancer research : MCR 20140728 12

<h4>Unlabelled</h4>Soft tissue sarcomas (STS) are malignant tumors of mesenchymal origin. A substantial portion of these tumors exhibits complex karyotypes and lack characterized chromosomal aberrations. Owing to such properties, both histopathologic and molecular classification of these tumors has been a significant challenge. This study examines the protein expression of a large number of human STS, including subtype heterogeneity, using two-dimensional gel proteomics. In addition, detailed pr ...[more]

PMID: 25069693

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Discovery-Based Protein Expression Profiling Identifies Distinct Subgroups and Pathways in Leiomyosarcomas

Project description:20 tumor samples run in duplicates, consisting of pleomorphic sarcomas; classfied as leiomyosarcoma or high-grade undifferentiated pleomorphic sarcoma.

2020-01-27 | PXD000616 | Pride

Transcription profiling by array of undifferentiated and differentiated human soft tissue sarcomas isolated from adipose tissue

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Proliferation and Tumorigenesis of a Murine Sarcoma Cell Line in the Absence of Dicer

Project description:MicroRNAs are a class of short ~22 nucleotide RNAs predicted to regulate nearly half of all protein-coding genes, including many involved in basal cellular processes and organismal development. Although both increases and decreases in the levels of specific miRNAs have been shown to promote tumor development, a global reduction in miRNAs is commonly observed in various human tumors. However, complete loss has not been documented, suggesting an essential function for miRNAs in tumorigenesis. Here we present the finding that transformed or immortalized Dicer-null somatic cells can be isolated readily in vitro, maintain the characteristics of Dicer-expressing controls and remain stably proliferative. Furthermore, Dicer-null cells from a sarcoma cell line, though depleted of miRNAs, are competent for tumor formation. Hence, miRNA levels in cancer may be maintained in vivo by a complex stabilizing selection in the intratumoral environment. Small RNAs from tumor cell lines (murine sarcoma KrasG12D, p53 -/-) with and without Dicer (Dicer f/-, Dicer -/-) were analyzed.

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ArrayCGH study to investigate duplication of T locus in chordoma

Project description:Duplication of T is a known familial susceptibility determinant for chordoma. TO determine if a similar genetic alteration occurs in the sporadic disease a high-resolution array-CGH (Agilent custom-designed arrayCGH chip) was used to interrogate the chr 6q27 locus for duplication of T. Twenty two samples of chordoma and reference genomic DNA were hybridised to the chip including a positive control from a chordoma cell line.

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Transcriptomic analysis of 162 myxofibrosarcomas and undifferentiated pleomorphic sarcomas

Project description:The global gene expression profiles of 162 myxofibrosarcomas and undifferentiated pleomorphic sarcomas were studied by RNA-sequencing. The profiles were compared with clinical and genomic features. 21 soft tissue tumors of other histotypes were used as out-group.

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Signaling pathways altered at the mitotic spindle in clathrin depleted cells

Project description:We present a snapshot of the regulation of mitotic-spindle proteins and their phosphorylation status in the absence of clathrin during metaphase. A reference list of proteins and phosphosites identified from a mitotic spindle preparation was generated using a label-free and a parallel chemical dimethyl isotopic peptide labelling approach. We further designed experiments to analyse proteins and phosphosites at the mitotic spindle whose abundance was affected by the knock-down of clathrin. We used dimethylation labelling of peptides in combination with fractionation strategies to identify and quantify phosphopeptides enriched by TiO2 beads and the flow-through non-phoshopeptides by ESI-LC-MS/MS for a broad coverage of the mitotic spindle proteome in the absence of clathrin.

2016-05-17 | PXD001603 | Pride

Transcription profiling of synovial sarcoma-like tumors induced in a genetically engineered mouse model

Project description:Synovial sarcoma-like tumors were generated in mice by conditionally expressing the human t(X;18) translocation-derived SYT-SSX2 fusion protein. Using a Tamoxifen-inducible CreER system, we show here that sporadic expression of SYT-SSX2 across multiple tissue types leads to exclusive formation of synovial sarcoma-like tumors while its widespread expression is lethal. CreER-based sporadic expression both avoids the severe early developmental phenotypes associated with widespread SYT-SSX2 expression and better models natural pathogenesis of cancers where transformed cells usually arise within an environment of largely normal cells. Experiment Overall Design: Genetically engineered mice capable of conditionally expressing the human synovial sarcoma-associated SYT-SSX2 fusion oncogene were mated with genetically engineered mice expressing the CreER fusion protein from ROSA locus. The progenies harboring both CreER and SYT-SSX2 were followed up with or without tamoxifen injection. Tumors were generated in these mice that were dissected out, RNA extracted, and subjected to expression profiling by microarray analysis.

2009-04-24 | E-GEOD-14469 | biostudies-arrayexpress

Clinical implications and molecular features of extracellular matrix networks in soft tissue sarcomas

Project description:The landscape of extracellular matrix (ECM) alterations in soft tissue sarcomas (STS) remains poorly characterised. We aimed to investigate the tumour ECM and adhesion signalling networks present in STS and their clinical implications.

2024-05-07 | PXD049373 | Pride

In vivo gene expression changes in EW5 Ewing sarcoma xenografts after IGF-1R or mTOR blockade

Project description:Ewing Sarcoma is caused by a pathognomonic genomic translocation that places an N-terminal EWSR1 gene in approximation with one of several ETS genes (typically FLI1). This aberration, in turn, alters the transcriptional regulation of more than five hundred genes and perturbs a number of critical pathways that promote oncogenesis, cell growth, invasion, and metastasis. Among them, translocation-mediated up-regulation of the insulin-like growth factor receptor 1 (IGF-1R) and mammalian target of rapamycin (mTOR) are of particular importance since they work in concert to facilitate IGF-1R expression and ligand-induced activation, respectively, of proven importance in ES transformation. When used as a single agent in Ewing sarcoma therapy, IGF-1R or mTOR inhibition leads to rapid counter-regulatory effects that blunt the intended therapeutic purpose. Therefore, identify new mechanisms of resistance that are used by Ewing sarcoma to evade cell death to single-agent IGF-1R or mTOR inhibition might suggest a number of therapeutic combinations that could improve their clinical activity. Male non-obese diabetic (NOD)-SCID-IL-2Rgnull mice were used to generate EW5 explants (2 mm). Mice bearing subcutaneous tumors were randomized into treatment and control groups when their tumors reached a diameter of 6 mm and received MK-8669 (mTOR inhibitor, 5mg/kg per dose, once weekly), MK-0646 (IGF-1R inhibitor monoclonal antibody, 0.5mg IP twice weekly), or a placebo control (sterile buffer). Animals were treated either until their tumors reached 1500 mm3 in volume. Affymetrix Geneship profiling of EW5 xenografts treated in vivo either with MK-0646, MK-8669, and control and compared each other using extracted RNA and hybridized on Affymetrix microrrays ( Affymetrix Human Genome U133A 2.0 cartridge arrays).

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