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AO-A0JE-01A_A2-A0T2-01A_AN-A0AJ-01A_phospho

ABSTRACT: TCGA Cancer Proteome Study of Breast Tissue, Phospho Enrichment, iTRAQ, AO-A0JE-01A_A2-A0T2-01A_AN-A0AJ-01A

INSTRUMENT(S): QExactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Breast

DISEASE(S): Breast Carcinoma

SUBMITTER: Nathan J. Edwards

PROVIDER: PAe004807 | PeptideAtlas | 2015-12-31

REPOSITORIES: PeptideAtlas

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			Action	DRS
	PAe004807_10247_tandem.params	Other
	PAe004807_README	Other
	PAe004807_Search_Results_10247_201512191515.properties	Other
	PAe004807_Search_Results_10247_201512191515.tar.gz	Other
	PAe004807_mzXML_201512191511.properties	Other

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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]

PMID: 25873244

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AO-A0JE-01A_A2-A0T2-01A_AN-A0AJ-01A

Project description:TCGA Cancer Proteome Study of Breast Tissue, iTRAQ, AO-A0JE-01A_A2-A0T2-01A_AN-A0AJ-01A

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Recurrent TCF12 mutations in anaplastic oligodendroglioma

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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An expression profiling study of anaplastic oligodendroglioma

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