Integrative Analysis of Complex Cancer Genomics and Clinical Profiles Using the cBioPortal
Open accessAbstract
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, occurring in approximately 60% of all glioblastoma cases.
“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]
In Instructions > Viewing and Interpreting the Results (page not specified), the paper says most CDKN2A alterations in its GBM example are homozygous deletions. It discusses CDKN2A as an RB-pathway gene, however, and does not establish that CDKN2A/ARF deletion is the most frequent p53-pathway alteration or occurs in approximately 60% of all GBM cases. Its 71% figure refers to alterations in any of three RB-pathway genes in the queried cases. (LLM, conf=0.88)
Experimental — accuracy not yet measuredPublicly available gene expression data from a matched cohort of mCRPC was downloaded from cBioportal.
“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]
IMP2 is genomically altered in over 2% of all cancers, which is above the baseline of random alterations in the average passenger genes.
“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]
The ‘Performing Cross-Cancer Queries’ section explains how cBioPortal displays alteration frequencies across cancer types, but gives no result for IMP2. Searches for IMP2, IGF2BP2, the over-2% figure, and a passenger-gene baseline found no passage establishing the claimed comparison. (LLM, conf=0.76)
Experimental — accuracy not yet measuredGenomic amplifications creating extra copies of IGF2BP2 occur in 9% of lung cancers.
“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]
The Viewing and Interpreting the Results section discusses copy-number amplification, but its examples concern ERBB2 in colorectal cancer and CDK4 in glioblastoma. Searches for IGF2BP2 and for a 9% amplification rate in lung cancer found no passage reporting the claimed finding. (LLM, conf=0.76)
Experimental — accuracy not yet measuredKRAS mutations are implicated in 25-30% of all human cancers, about 19% of non-small cell lung cancers, about 40% of colorectal cancers, and about 73% of pancreatic ductal adenocarcinoma cases.
“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]
The Instructions > Viewing and Interpreting the Results section describes how cBioPortal displays mutation frequencies, but does not report KRAS prevalence in all cancers, NSCLC, colorectal cancer, or PDAC. Searches for KRAS and the cited percentages found no passage in our copy supporting those figures. (LLM, conf=0.75)
Experimental — accuracy not yet measured
TP53 is deregulated in 22% of glioblastomas, while ARF, MDM2, and MDM4 are deregulated in 61%, 10%, and 10% of glioblastomas, respectively.
“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]
The Instructions sections use GBM to illustrate alterations in RB-pathway genes and use TP53 to illustrate cross-cancer queries, but neither passage gives the claimed GBM frequencies. Searches for ARF, MDM4, and the stated percentages found no passage in our copy reporting them. (LLM, conf=0.74)
Experimental — accuracy not yet measuredStudies have shown that STK11 loss-of-function mutations result in epigenetic changes that lead to silencing of immune genes.
“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 <i>STK11</i> -Mutant Tumors to Anti–PD-1 Immunotherapy (2025) · cites this paper as [3]
The Instructions section describes how cBioPortal displays mutations, DNA methylation, and other data, but does not report an STK11 finding. Searches for STK11 loss-of-function, epigenetic changes, and immune-gene silencing found no passage in our copy addressing the claimed causal link; page numbers were not provided. (LLM, conf=0.78)
Experimental — accuracy not yet measuredIn patients with HCC, high PROX1 expression is associated with increased survival.
“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]
The Instructions section, under Viewing and Interpreting the Results (page unavailable), reports a survival association for BRCA1/BRCA2 mutations in ovarian cancer, not PROX1 expression in HCC. Searches for PROX1, HCC and hepatocellular-carcinoma survival found no passage in our copy addressing the claimed association. (LLM, conf=0.77)
Experimental — accuracy not yet measuredIn patients with HCC, chromosomal amplifications including PROX1 are associated with increased survival.
“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]
The Viewing and Interpreting the Results section describes survival analysis using BRCA1/BRCA2 mutations in ovarian cancer, not PROX1 amplification in HCC. Searches for PROX1 and for hepatocellular carcinoma or liver cancer found no passage addressing the claimed survival association in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredCancer samples often carry mutations in BRCA1 residues 758-1064.
“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]
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.
“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]
Frequently co-altered genes in KRAS G12C mutated NSCLC include TP53, STK11, KEAP1, and CDKN2A.
“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]
Analysis of TCGA data shows that a fraction of multiple cancers have overexpressed MDMX concurrently with inactivated p53.
“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 TCGA data, squamous cell carcinoma of the lung or head and neck co-inactivated ARF and TP53 in about 20% of tumors.
“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
Only a small fraction of analyzed tumors, 0.84% (18 of 2148), carried p21 deletions or mutations.
“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 authors' TCGA analysis, up to 6% of specific human malignancies had amplified MDM2 or MDM4 together with TP53 mutations.
“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 authors' TCGA evaluation, USP7 was rarely amplified in human cancer.
“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
More than 6% of specific human malignancies had increased MDM2 or MDM4 mRNA expression together with TP53 mutations.
“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 TCGA data, 5.3% of breast adenocarcinomas had amplified USP7, and 75% of those tumors retained wild-type TP53 allele status.
“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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- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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