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Integrative Analysis of Complex Cancer Genomics and Clinical Profiles Using the cBioPortal
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The cBioPortal enables integration, visualization, and analysis of multidimensional cancer genomic and clinical data.
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“The most frequently deregulated component of the p53 pathway is a homozygous deletion of the CDKN2A/ARF locus, which occurs in ~60% of all GBM cases (Figure 1) [22,23].”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [23]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Publicly available gene expression data from a matched cohort established previously59 or mCRPC was downloaded from cBioportal (20 May 2021)94–96.”
From Genome-scale CRISPR screens identify PTGES3 as a direct modulator of androgen receptor function in advanced prostate cancer (2025) · cites this paper as [96]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“IMP2 is genomically altered in over 2% of all cancers, which is above the baseline of random alterations in the average passenger genes (Figure 5A) [77,78,79].”
From IMPlications of IMP2 in RNA Biology and Disease (2025) · cites this paper as [78]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Genomic amplifications creating extra copies of IGF2BP2 occur in 9% of lung cancers (Figure 5A) [77,78,79].”
From IMPlications of IMP2 in RNA Biology and Disease (2025) · cites this paper as [78]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
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“KRAS mutations are implicated in 25–30% of all human cancers, about 19% of non-small cell lung cancers (NSCLCs), about 40% of colorectal cancers (CRCs), and about 73% of pancreatic ductal adenocarcinoma (PDAC) cases (Figure 1) [1,2].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [2]
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“TP53 is deregulated in 22% of GBMs, while ARF, MDM2, and MDM4 are deregulated in 61%, 10%, and 10% of GBMs, respectively (Figure 1) [22,23].”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [23]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
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“Indeed, studies have shown that STK11 loss-of-function mutations result in epigenetic changes that lead to silencing of immune genes (3, 13).”
From TNG260 Is a Small-Molecule CoREST Inhibitor That Sensitizes STK11 -Mutant Tumors to Anti–PD-1 Immunotherapy (2025) · cites this paper as [3]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
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“in patients with HCC, high PROX1 expression or chromosomal amplifications including PROX1 were both associated with increased survival25–32”
From Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis (2025) · cites this paper as [27]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“in patients with HCC, high PROX1 expression or chromosomal amplifications including PROX1 were both associated with increased survival25–32”
From Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis (2025) · cites this paper as [27]
Experimental — accuracy not yet measuredIn the citing paper
“We note that the region of BRCA1 (amino acid residues 758-1064) that harbors the RAD51 interaction domain17 is frequently mutated in cancer (cBioPortal for Cancer Genomic)44,45”
From BRCA1–BARD1 promotes RAD51-mediated homologous DNA pairing (2017) · cites this paper as [45]
In the citing paper
“Based on non-small cell lung cancer datasets within cBioPortal, the landscape of KRAS G12C mutated tumors includes a complex landscape of co-altered genes (Fig. 3)25,26.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [26]
In the citing paper
“Frequently co-altered genes include TP53, STK11, KEAP1, and CDKN2A.”
From Selective KRAS G12C inhibitors in non-small cell lung cancer: chemistry, concurrent pathway alterations, and clinical outcomes (2021) · cites this paper as [26]
In the citing paper
“Analysis of the data in The Cancer Genome Atlas provides further evidence that a certain fraction of multiple cancers have overexpressed MDMX (amplification or mRNA) concurrently with inactivated (mutated or deleted) p53 (Table 1;34,35).”
From Mdmx promotes genomic instability independent of p53 and Mdm2 (2015) · cites this paper as [35]
In the citing paper
“For example, we evaluated ARF and TP53 status in the data from The Cancer Genome Atlas (TCGA) and determined that malignancies such as squamous cell carcinoma of the lung or head and neck co-inactivate ARF and TP53 in approximately 20% of these tumors (Table 1; (Cerami, et al., 2012; Gao, et al., 2013).”
From The Mdm network and its regulation of p53 activities: a rheostat of cancer risk (2014) · cites this paper as Gao, et al., 2013
In the citing paper
“0.84% (18 of 2148) tumors analyzed had p21 deletions or mutations (Cerami, et al., 2012; Gao, et al., 2013).”
From The Mdm network and its regulation of p53 activities: a rheostat of cancer risk (2014) · cites this paper as Gao, et al., 2013
In the citing paper
“Our analysis of TCGA data showed that up to 6% of specific human malignancies have amplified MDM2 or MDM4 (and even more have increased MDM2 or MDM4 mRNA expression) with concomitant TP53 mutations”
From The Mdm network and its regulation of p53 activities: a rheostat of cancer risk (2014) · cites this paper as Gao, et al., 2013
In the citing paper
“Our evaluation of TCGA data revealed that USP7 is rarely amplified in human cancer (Cerami, et al., 2012; Gao, et al., 2013).”
From The Mdm network and its regulation of p53 activities: a rheostat of cancer risk (2014) · cites this paper as Gao, et al., 2013
In the citing paper
“even more have increased MDM2 or MDM4 mRNA expression”
From The Mdm network and its regulation of p53 activities: a rheostat of cancer risk (2014) · cites this paper as Gao, et al., 2013
In the citing paper
“However, 5.3% (40 of 760) of breast adenocarcinomas contained amplified USP7 and of those, 75% maintained wild-type TP53 allele status, which implies that USP7 may have other functions related to oncogenesis.”
From The Mdm network and its regulation of p53 activities: a rheostat of cancer risk (2014) · cites this paper as Gao, et al., 2013
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Metadata
- Authors
- Gao, J., Aksoy, B. A., Dogrusoz, U., Dresdner, G., Gross, B., Sumer, S. O., Sun, Y., Jacobsen, A., Sinha, R., Larsson, E., Cerami, E., Sander, C., & Schultz, N.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Computer Engineering Department, Bilkent University, 06800 Ankara, Turkey.
- Computational Biology Center, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
- University of Gothenburg (SE)
- ORCID
- Venue
- Science Signaling
- Published
- 2013-04-02
- Volume
- 6
- Issue
- 269
- Pages
- pl1-pl1
- ISSN
- 1937-9145 (ISSN-L)
- 1945-0877
- PMC
- PMC4160307
- OpenAlex
- W2114843025
- Semantic Scholar
- 99649284503c2abe6871ae45f3dbf394a3a86352
- Cited by
- 15,160
- References
- 36
- Citations by year
- 2026: 671 · 2025: 1105 · 2024: 1485 · 2023: 1699 · 2022: 1862 · 2021: 1934 · 2020: 1747 · 2019: 1345 · 2018: 989 · 2017: 898 · 2016: 684 · 2015: 494 · 2014: 196 · 2013: 33
- FWCI
- 164.92
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Signaling (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Bilkent University Institutional Repository (Bilkent University) (submittedVersion)
- Funders
- National Cancer Institute (R01CA132744, U24CA143840, R21CA135870)
- National Institute of General Medical Sciences (GM 103504, P41GM103504)
- National Center for Research Resources (P41RR031228)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bioinformatics and Genomic Networks
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- cBioPortal, cancer genomics, clinical outcomes, gene expression profiling, proteomics, epigenetics, network visualization, survival analysis
- MeSH terms
- Humans, Neoplasms, Software, Reproducibility of Results, Information Storage and Retrieval, Genetic Predisposition to Disease, Internet, Gene Expression Profiling, Genomics, Gene Regulatory Networks
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