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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    • "The same genes were similarly queried from microarray-based gene expression profiling of 11 commonly used prostate cancer cell lines, and from RNAseq data in the Robinson et al. CRPC profiling study[22](downloaded from cBioPortal[23]). "
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    ABSTRACT: A recent phase III trial of the MET kinase inhibitor cabozantinib in men with castration-resistant prostate cancer (CRPC) failed to meet its primary survival end point; however, most men with CRPC have intact androgen receptor (AR) signaling. As previous work supports negative regulation of MET by AR signaling, we hypothesized that intact AR signaling may have limited the efficacy of cabozantinib in some of these patients. To assess the role of AR signaling on MET inhibition, we first performed an in silico analysis of human CRPC tissue samples stratified by AR signaling status (+ or −), which identified MET expression as markedly increased in AR− samples. In vitro, AR signaling inhibition in AR+ CRPC models increased MET expression and resulted in susceptibility to ligand (HGF) activation. Likewise, MET inhibition was only effective in blocking cancer phenotypes in cells with MET overexpression. Using multiple AR+ CRPC in vitro and in vivo models, we showed that combined cabozantinib and enzalutamide (AR antagonist) treatment was more efficacious than either inhibitor alone. These data provide a compelling rationale to combine AR and MET inhibition in CRPC and may explain the negative results of the phase III cabozantinib study in CRPC. Similarly, the expression of MET in AR− disease, whether due to AR inhibition or loss of AR signaling, suggests potential utility for MET inhibition in select patients with AR therapy resistance and in AR− prostate cancer.
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    • "Most interestingly, ELF3 a transcriptional regulator of TGFBR2 was mutated in 10.6% of the periampullary tumors with predominantly inactivating frameshift or nonsense mutations (Figure 3B). This mutation frequency is three times higher than in any other cancer (Table S3D) (Cerami et al., 2012;Gao et al., 2013;Lawrence et al., 2014) ( In agreement with our finding, ELF3 mutations were found in 9.5% of extrahepathic CAC in a recent study of 74 samples with four inactivating mutations out of seven (Nakamura et al., 2015). "
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    ABSTRACT: The ampulla of Vater is a complex cellular environment from which adenocarcinomas arise to form a group of histopathologically heterogenous tumors. To evaluate the molecular features of these tumors, 98 ampullary adenocarcinomas were evaluated and compared to 44 distal bile duct and 18 duodenal adenocarcinomas. Genomic analyses revealed mutations in the WNT signaling pathway among half of the patients and in all three adenocarcinomas irrespective of their origin and histological morphology. These tumors were characterized by a high frequency of inactivating mutations of ELF3, a high rate of microsatellite instability, and common focal deletions and amplifications, suggesting common attributes in the molecular pathogenesis are at play in these tumors. The high frequency of WNT pathway activating mutation, coupled with small-molecule inhibitors of β-catenin in clinical trials, suggests future treatment decisions for these patients may be guided by genomic analysis.
    Full-text · Article · Jan 2016 · Cell Reports
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    • "All samples were processed as a part of the U.S. national TCGA initiative to quantitatively characterize over 80 forms of cancer at the molecular level. Information was gathered and graphed by the cBioPortal site [Cerami, Gao et al., 2012; Gao et al., 2013]. "
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    DESCRIPTION: Myeloid zinc finger 1 (MZF1) belongs to the SCAN-Zinc Finger (SCAN-ZF) transcription factor family that has recently been implicated in a number of types of cancer. Although the initial studies concentrated on the role of MZF1 in myeloid differentiation and leukemia, the factor now appears to be involved in the etiology of major solid tumors such as lung, cervical, breast, and colorectal cancer. Here we discuss the regulation of MZF1 that mediated its recruitment and activation in cancer, concentrating on posttranslational modification by phosphorylation, and sumoylation, formation of promyelocytic leukemia nuclear bodies and its association with co-activators and corepressors. J. Cell. Biochem. 116: 2146–2154, 2015.
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