This tab shows an overview of the selected study/paper [more details]
Reference

The genomic complexity of primary human prostate cancer.

Paper Id
COSP25499
Authors
Berger MF,Lawrence MS,Demichelis F,Drier Y,Cibulskis K,Sivachenko AY,Sboner A,Esgueva R,Pflueger D,Sougnez C,Onofrio R,Carter SL,Park K,Habegger L,Ambrogio L,Fennell T,Parkin M,Saksena G,Voet D,Ramos AH,Pugh TJ,Wilkinson J,Fisher S,Winckler W,Mahan S,Ardlie K,Baldwin J,Simons JW,Kitabayashi N,MacDonald TY,Kantoff PW,Chin L,Gabriel SB,Gerstein MB,Golub TR,Meyerson M,Tewari A,Lander ES,Getz G,Rubin MA and Garraway LA
Affiliation
The Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA.
Journal
Nature 2011;470(7333):214-20
ISSN:1476-4687
PUBMED:21307934
Abstract
Prostate cancer is the second most common cause of male cancer deaths in the United States. However, the full range of prostate cancer genomic alterations is incompletely characterized. Here we present the complete sequence of seven primary human prostate cancers and their paired normal counterparts. Several tumours contained complex chains of balanced (that is, 'copy-neutral') rearrangements that occurred within or adjacent to known cancer genes. Rearrangement breakpoints were enriched near open chromatin, androgen receptor and ERG DNA binding sites in the setting of the ETS gene fusion TMPRSS2-ERG, but inversely correlated with these regions in tumours lacking ETS fusions. This observation suggests a link between chromatin or transcriptional regulation and the genesis of genomic aberrations. Three tumours contained rearrangements that disrupted CADM2, and four harboured events disrupting either PTEN (unbalanced events), a prostate tumour suppressor, or MAGI2 (balanced events), a PTEN interacting protein not previously implicated in prostate tumorigenesis. Thus, genomic rearrangements may arise from transcriptional or chromatin aberrancies and engage prostate tumorigenic mechanisms.
Paper Status
Curated
Genes Analysed
2155
Mutated Samples
7
Total No. of Samples
7
This tab shows genes with mutations in the selected study/paper [more details]
Genes Samples CDS Mutation AA Mutation
This tab shows genes without mutations in the selected study/paper [more details]
Non-Mutant Genes Gene Id (COSG)
This tab shows samples without mutations in the selected study/paper [more details]
Non-Mutant Samples Sample Id (COSS)
This tab shows mutated samples in the selected study/paper [more details]
Sample Name Mutation Count
This tab shows non coding variant in the selected study/paper [more details]
Sample ID Sample Name ID NCV Annotation Zygosity Chromosome Genome start Genome stop Genome version Strand WT seq Mut seq
This tab shows the copy number variation data for this study. Only variants (classified as gain or loss) are listed. [more details]
CNV Gene Sample Position Minor Allele Copy Number Average Ploidy

1. N/A represents cases where average ploidy value is not available( mostly ICGC samples). For some TCGA samples where minor allele information is not available the average ploidy value could not be calculated.

2. For TCGA samples, Ascat algorithm is used to calculate the average ploidy.

3. For CGP samples, Picnic algorithm is used to calculate the average ploidy.

Type
This tab shows a table of count of samples having gain or loss for all genes [more details]
Gene Gain Samples Loss Samples Samples Tested
This tab shows the fusion mutations observed in this sample [more details]
Gene Sample Name Id Sample(COSS) CDS Mutation Somatic status Zygosity Validated Type