AO-A12D-01A_AN-A04A-01A_BH-A0AV-01A_phospho
Ontology highlight
ABSTRACT:
INSTRUMENT(S): QExactive
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Breast
DISEASE(S): Breast Carcinoma
SUBMITTER: Nathan J. Edwards
PROVIDER: PAe004769 | PeptideAtlas | 2015-12-31
REPOSITORIES: PeptideAtlas
Dataset's files
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Publications
The CPTAC Data Portal: A Resource for Cancer Proteomics Research.
Edwards Nathan J NJ Oberti Mauricio M Thangudu Ratna R RR Cai Shuang S McGarvey Peter B PB Jacob Shine S Madhavan Subha S Ketchum Karen A KA
Journal of proteome research 20150504 6
The Clinical Proteomic Tumor Analysis Consortium (CPTAC), under the auspices of the National Cancer Institute's Office of Cancer Clinical Proteomics Research, is a comprehensive and coordinated effort to accelerate the understanding of the molecular basis of cancer through the application of proteomic technologies and workflows to clinical tumor samples with characterized genomic and transcript profiles. The consortium analyzes cancer biospecimens using mass spectrometry, identifying and quantif ...[more]
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Project description:<a href="https://pdc.esacinc.com/pdc/browse/filters/study_name:TCGA_Breast_Cancer_Proteome|TCGA_Breast_Cancer_Phosphoproteome" target="_blank">Explore This Study at the NCI Proteomic Data Commons</a><p>Global proteome and phosphoproteome data have been acquired for 105 TCGA breast cancer samples using iTRAQ (isobaric Tags for Relative and Absolute Quantification) protein quantification methods. Samples were selected from each of the 4 breast tumor subtypes (Luminal A, Luminal B, Basal-like, HER2-enriched) described in the publication, <a href="http://www.ncbi.nlm.nih.gov/pubmed/23000897" target="_blank">Comprehensive molecular portraits of human breast tumors (Cancer Genome Atlas Network, Nature 2012)</a>.</p><p>Three TCGA samples and 1 common internal reference control sample are included in each iTRAQ experiment, consisting of 25 proteome and 13 phosphoproteome files. The internal reference is comprised of a mixture of 40 TCGA samples (of the 105 breast cancer samples) with equal representation of the 4 breast subtypes. Three of the TCGA samples have been assayed in duplicate for quality control purposes.</p><p>05TCGA_AO-A12D-01A_AN-A04A-01A_BH-A0AV-01A_Proteome_BI iTRAQ proteome data were acquired twice, before (20130310) and after (20130416) maintenance of the Q Exactive MS system. The "20130416" dataset was used in the final publication (see <a href="https://cptac-data-portal.georgetown.edu/cptac/s/S029" target="_blank">here</a>).</p><p>Global proteome and phosphoproteome data were acquired for three normal breast samples in Experiment 37. Samples "263d3f-I", "blcdb9-I", and "c4155b-C" are normal breast tissue samples that were measured in the iTRAQ-114, -115, and -116 channels, respectively. All normal samples were compared to the internal reference sample in the iTRAQ-117 channel (see CPTAC, TCGA Breast Cancer iTRAQ Sample Mapping file below).</p><p>Information on the complete TCGA Breast invasive carcinoma cohort (BRCA) can be found <a href="https://portal.gdc.cancer.gov/projects/TCGA-BRCA" target="_blank">here</a>.<br/>Genomic data for the 105 TCGA samples used in the CPTAC Proteome study can be downloaded from <a href="https://portal.gdc.cancer.gov/legacy-archive/search/f?filters=%7B%22op%22:%22and%22,%22content%22:%5B%7B%22op%22:%22in%22,%22content%22:%7B%22field%22:%22cases.project.program.name%22,%22value%22:%5B%22TCGA%22%5D%7D%7D,%7B%22op%22:%22in%22,%22content%22:%7B%22field%22:%22cases.project.project_id%22,%22value%22:%5B%22TCGA-BRCA%22%5D%7D%7D%5D%7D" target="_blank">here</a>.</p><ul><li>Dataset imported into MassIVE from <a href="https://cptac-data-portal.georgetown.edu/cptac/s/S015">https://cptac-data-portal.georgetown.edu/cptac/s/S015</a> on 10/15/18</li><li>Dataset source: <a href="https://pdc.esacinc.com/pdc/browse/filters/study_name:TCGA_Breast_Cancer_Proteome|TCGA_Breast_Cancer_Phosphoproteome" target="_blank">https://pdc.esacinc.com/pdc/browse/filters/study_name:...</a></li></ul>
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2015-12-31 | PAe004820 | PeptideAtlas
Project description:<a href="https://pdc.esacinc.com/pdc/browse/filters/study_name:TCGA_Breast_Cancer_Proteome|TCGA_Breast_Cancer_Phosphoproteome" target="_blank">Explore This Study at the NCI Proteomic Data Commons</a><p><a href="http://www.nature.com/nature/journal/vaop/ncurrent/full/nature18003.html" target="_blank">Mertins P, Mani DR, Ruggles KV, Gillette MA, Clauser KR, Wang P et al., Nature (2016) doi:10.1038/nature18003 Published online 25 May 2016</a></p><p>Somatic mutations have been extensively characterized in breast cancer, but the effects of these genetic alterations on the proteomic landscape remain poorly understood. Here we describe quantitative mass-spectrometry-based proteomic and phosphoproteomic analyses of 105 genomically annotated breast cancers, of which 77 provided high-quality data. Integrated analyses provided insights into the somatic cancer genome including the consequences of chromosomal loss, such as the 5q deletion characteristic of basal-like breast cancer. Interrogation of the 5q trans-effects against the Library of Integrated Network-based Cellular Signatures, connected loss of CETN3 and SKP1 to elevated expression of epidermal growth factor receptor (EGFR), and SKP1 loss also to increased SRC tyrosine kinase. Global proteomic data confirmed a stromal-enriched group of proteins in addition to basal and luminal clusters, and pathway analysis of the phosphoproteome identified a G-protein-coupled receptor cluster that was not readily identified at the mRNA level. In addition to ERBB2, other amplicon-associated highly phosphorylated kinases were identified, including CDK12, PAK1, PTK2, RIPK2 and TLK2. 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Project description:A Cartes d'Identite des Tumeurs (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net: Anaplastic oligodendrogliomas (AOs) are rare primary brain tumors which are generally incurable with few treatment targets identified. Most oligodendrogliomas have chromosome 1p/19q co-deletion and IDH mutation. We analyzed 51 AOs by whole-exome and/or transcriptome sequencing identifying previously reported frequent somatic mutations in CIC and FUBP1 genes. We also identified recurrent mutations in TCF12 (11% of IDHmut-codel) which encodes basic helix-loop-helix (bHLFH) transcription factor 12 which is an oligodendrocyte-related transcription factor in IDHmut-codel tumors. Strikingly, the somatic mutations (encoding E548R and R602M substitutions) have not been reported previously in cancer but are identical to germline mutations causing craniosynostosis. Incorporating TCGA data on 43 AO tumors also implicates functional mutation of SMARCA4, NOTCH1, NOTCH2, SETD2, RBPJ and ARID1A/1B. These data are compatible with the combined deregulation of metabolism, chromatin organization/remodeling and Notch-pathway genes in AO oncogenesis. Our analysis provides further insights into the unique and shared pathways driving AO and new targets for therapeutic intervention.
2015-06-15 | E-MTAB-2767 | biostudies-arrayexpress
Project description:A Cartes d'Identite des Tumeurs (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net): Anaplastic oligodendrogliomas (AOs) are rare primary brain tumors which are generally incurable with few treatment targets identified. Most oligodendrogliomas have chromosome 1p/19q co-deletion and IDH mutation. We analyzed 51 AOs by whole-exome and/or transcriptome sequencing identifying previously reported frequent somatic mutations in CIC and FUBP1 genes. We also identified recurrent mutations in TCF12 (11% of IDHmut-codel) which encodes basic helix-loop-helix (bHLFH) transcription factor 12; which is an oligodendrocyte-related transcription factor in IDHmut-codel tumors. Strikingly, the somatic mutations (encoding E548R and R602M substitutions) have not been reported previously in cancer but are identical to germline mutations causing craniosynostosis. Incorporating TCGA data on 43 AO tumors also implicates functional mutation of SMARCA4, NOTCH1, NOTCH2, SETD2, RBPJ and ARID1A/1B. These data are compatible with the combined deregulation of metabolism, chromatin organization/remodeling and Notch-pathway genes in AO oncogenesis. Our analysis provides further insights into the unique and shared pathways driving AO and new targets for therapeutic intervention.
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