The cBio Cancer Genomics Portal: An Open Platform for Exploring Multidimensional Cancer Genomics Data

Computational Biology Center, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.
Cancer Discovery (Impact Factor: 19.45). 05/2012; 2(5):401-4. DOI: 10.1158/2159-8290.CD-12-0095
Source: PubMed


The cBio Cancer Genomics Portal ( is an open-access resource for interactive exploration of multidimensional cancer genomics data sets, currently providing access to data from more than 5,000 tumor samples from 20 cancer studies. The cBio Cancer Genomics Portal significantly lowers the barriers between complex genomic data and cancer researchers who want rapid, intuitive, and high-quality access to molecular profiles and clinical attributes from large-scale cancer genomics projects and empowers researchers to translate these rich data sets into biologic insights and clinical applications.

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Available from: Erik Larsson Lekholm,
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    • "Genomic loss of at least one copy of RBPJ was associated with significantly reduced transcript levels in primary lung tumors (Fig. 1 G; Lockwood et al., 2008; Lockwood et al., 2010). Classification of tumors in Fig. 1 G into subtypes showed that RBPJ copy number loss occurred more frequently in lung squamous cell carcinomas compared with adenocarcinomas, consistent with our analysis of TCGA lung tumor data (Fig. 1, H and I; Cerami et al., 2012; Lockwood et al., 2012; Gao et al., 2013). Examination of 215 different tumor cell lines representing 15 tumor types showed that deletion of at least one copy of RBPJ occurred in 35% of all cell lines (Fig. 1 J and Table S1). "
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    ABSTRACT: Aberrant Notch activity is oncogenic in several malignancies, but it is unclear how expression or function of downstream elements in the Notch pathway affects tumor growth. Transcriptional regulation by Notch is dependent on interaction with the DNA-binding transcriptional repressor, RBPJ, and consequent derepression or activation of associated gene promoters. We show here that RBPJ is frequently depleted in human tumors. Depletion of RBPJ in human cancer cell lines xenografted into immunodeficient mice resulted in activation of canonical Notch target genes, and accelerated tumor growth secondary to reduced cell death. Global analysis of activated regions of the genome, as defined by differential acetylation of histone H4 (H4ac), revealed that the cell death pathway was significantly dysregulated in RBPJ-depleted tumors. Analysis of transcription factor binding data identified several transcriptional activators that bind promoters with differential H4ac in RBPJ-depleted cells. Functional studies demonstrated that NF-κB and MYC were essential for survival of RBPJ-depleted cells. Thus, loss of RBPJ derepresses target gene promoters, allowing Notch-independent activation by alternate transcription factors that promote tumorigenesis.
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    • "We analysed publically available cancer genome datasets at the cBioPortal for Cancer Genomics (Supplementary data) providing access to data from 20,958 tumour samples from 89 cancer studies (data available up to 21st January 2015) [22] [23] and data from the 1000 Genome project [24] [25] [26] to identify mutations, copy-number alterations and mRNA expression levels (using a mRNA expression z-score threshold value of ± 2.0). "
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    ABSTRACT: FAM72 is a novel neuronal progenitor cell (NPC) self-renewal supporting protein expressed under physiological conditions at low levels in other tissues. Accumulating data indicate the potential pivotal tumourigenic effects of FAM72. Our in silico human genome-wide analysis (GWA) revealed that the FAM72 gene family consists of four human-specific paralogous members, all of which are located on chromosome (chr) 1. Unique asymmetric FAM72 segmental gene duplications are most likely to have occurred in conjunction with the paired genomic neighbour SRGAP2 (SLIT-ROBO Rho GTPase activating protein), as both genes have four paralogues in humans but only one vertebra-emerging orthologue in all other species. No species with two or three FAM72/SRGAP2 gene pairs could be identified, and the four exclusively human-defining ohnologues, with different mutation patterns in Homo neanderthalensis and Denisova hominin, may remain under epigenetic control through long non-coding (lnc) RNAs.
    Genomics 10/2015; 106:278-285. · 2.28 Impact Factor
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    • "Consistent with IHC results, YAP was highly expressed in cervical cancer cell lines (ME180, HT3, and HeLa), while in Ect1 cells, an immortalized epithelial cell line derived from the ectocervical epithelium, YAP protein was expressed at low levels and was highly phosphorylated (Appendix Fig S1A). To confirm that YAP plays a role in human cervical cancer progression, we analyzed YAP gene alteration using data extracted from The Cancer Genomic Atlas (TCGA) database and the cBioPortal online analyzing tool (the cBioPortal for Cancer Genomics) (Cerami et al, 2012; Gao et al, 2013). The cross-cancer YAP alteration analysis shows that YAP is frequently altered in different types of cancers (Fig 1I). "
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    ABSTRACT: The Hippo signaling pathway controls organ size and tumorigene-sis through a kinase cascade that inactivates Yes-associated protein (YAP). Here, we show that YAP plays a central role in controlling the progression of cervical cancer. Our results suggest that YAP expression is associated with a poor prognosis for cervical cancer. TGF-a and amphiregulin (AREG), via EGFR, inhibit the Hippo signaling pathway and activate YAP to induce cervical cancer cell proliferation and migration. Activated YAP allows for up-regulation of TGF-a, AREG, and EGFR, forming a positive signaling loop to drive cervical cancer cell proliferation. HPV E6 protein, a major etiological molecule of cervical cancer, maintains high YAP protein levels in cervical cancer cells by preventing proteasome-dependent YAP degradation to drive cervical cancer cell proliferation. Results from human cervical cancer genomic databases and an accepted transgenic mouse model strongly support the clinical relevance of the discovered feed-forward signaling loop. Our study indicates that combined targeting of the Hippo and the ERBB signaling pathways represents a novel therapeutic strategy for prevention and treatment of cervical cancer.
    EMBO Molecular Medicine 09/2015; 7(11):e201404976. DOI:10.15252/emmm.201404976 · 8.67 Impact Factor
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