The DOI matches its Crossref record; 16 of the 17 references it cites were found in a registry or an index.
The cBio Cancer Genomics Portal: An Open Platform for Exploring Multidimensional Cancer Genomics Data
Open accessAbstract
The cBio Cancer Genomics Portal (http://cbioportal.org) 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. Cancer Discov; 2(5); 401–4. ©2012 AACR.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Second, cBioPortal and COSMIC are primarily focused on patient tumour genomic data.”
From Cell Model Passports-a hub for clinical, genetic and functional datasets of preclinical cancer models (2019) · cites this paper as [36]
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 [95]
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 [77]
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 [77]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“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 [1]
Experimental — accuracy not yet measured
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“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 [22]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“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 [22]
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 [26]
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 [26]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“The prevalence of STAT3 overactivation in cancer cannot be explained by mutational activation of STAT3 because somatic mutation of the STAT3 gene in cancer is rare (1.08%; 54/4980 tumors analyzed to date by whole exome sequencing by The Cancer Genome Atlas).38”
From Critical analysis of the potential for targeting STAT3 in human malignancy (2013) · cites this paper as [38]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“It is an important tumour suppressor gene mutated in 6% of colorectal cancers (CRCs), and germline variants in PTEN are causative of PTEN hamartoma tumour syndrome (Hobert and Eng, 2009; Cerami et al., 2012).”
From Efficient genetic editing of human intestinal organoids using ribonucleoprotein-based CRISPR (2023) · cites this paper as Cerami et al., 2012
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 [44]
In the citing paper
“Despite being the most frequently altered oncogenic protein in solid tumours, KRAS has historically been considered ‘undruggable’”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [17]
In the citing paper
“each dataset indicates that ~20% of all malignancies have a RAS abnormality. Overall, ~17% of solid tumours have KRAS mutations, including ~90% of pancreatic, ~50% of colon and ~25% of lung adenocarcinomas16,17”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [17]
In the citing paper
“KRAS mutations predominate in NSCLCs, accounting for ~78% of all RAS mutations found in such tumours17. The activating missense KRAS mutations that occur in ~25% of NSCLCs19–23 are typically mutually exclusive with other clinically actionable driver mutations, such as those in EGFR, BRAF and ALK24.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [17]
In the citing paper
“approximately one in seven of all human cancers harbor KRAS (Kirsten rat sarcoma virus) alterations”
From Expanding the Reach of Precision Oncology by Drugging All KRAS Mutants (2022) · cites this paper as [4]
In the citing paper
“KRAS is the most frequently mutated oncogene”
From Expanding the Reach of Precision Oncology by Drugging All KRAS Mutants (2022) · cites this paper as [4]
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 [25]
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 [25]
In the citing paper
“Within the KRAS mutant subgroup, lower RNA expression of PTK2 (FAK coding gene) correlates with better survival outcomes”
From Focal Adhesion Kinase (FAK) Inhibition Synergizes with KRAS G12C Inhibitors in Treating Cancer through the Regulation of the FAK–YAP Signaling (2021) · cites this paper as [19]
In the citing paper
“while for KRAS wild type subgroup, there is no difference between the PTK2 low and high expression groups (Figure 1A,B)”
From Focal Adhesion Kinase (FAK) Inhibition Synergizes with KRAS G12C Inhibitors in Treating Cancer through the Regulation of the FAK–YAP Signaling (2021) · cites this paper as [19]
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 [34]
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 Cerami, et al., 2012
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 Cerami, et al., 2012
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 Cerami, et al., 2012
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 Cerami, et al., 2012
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 Cerami, et al., 2012
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 Cerami, et al., 2012
In the citing paper
“First, Cellosaurus and cBioPortal do not provide cell model functional information, while PharmacoDB does not contain genomic annotation of the cell models and has limited sample/model information.”
From Cell Model Passports-a hub for clinical, genetic and functional datasets of preclinical cancer models (2019) · cites this paper as [36]
In the citing paper
“Third, neither cBioPortal, PharmacoDB nor COSMIC curate samples to map unique identifiers or link samples and models from the same patient, which can be important for identifying mis-identified or cross-contaminated samples.”
From Cell Model Passports-a hub for clinical, genetic and functional datasets of preclinical cancer models (2019) · cites this paper as [36]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Robinson, J. T., Thorvaldsdóttir, H., Winckler, W., Guttman, M., Lander, E. S., Getz, G., & Mesirov, J. P. (2011) · Nature Biotechnology · doi:10.1038/nbt.1754 · Cited by 15,390
The Pfam Protein Families Database
Bateman, A. G. (2002) · Nucleic Acids Research · doi:10.1093/nar/30.1.276 · Cited by 14,075
Integrated genomic analyses of ovarian carcinoma
Perou, C. M. (2019) · Carolina Digital Repository (University of North Carolina at Chapel Hill) · doi:10.17615/hvp3-wg08 · Cited by 7,927
Comprehensive genomic characterization defines human glioblastoma genes and core pathways
The Cancer Genome Atlas Research Network (2008) · Nature · doi:10.1038/nature07385 · Cited by 7,735
The Pfam protein families database
Punta, M., Coggill, P. C., Eberhardt, R. Y., Mistry, J., Tate, J., Boursnell, C., Pang, N., Forslund, K., Ceric, G., Clements, J., et al. (2012) · Nucleic Acids Research · doi:10.1093/nar/gkr1065 · Cited by 3,719
Integrative Genomic Profiling of Human Prostate Cancer
Taylor, B. S., Schultz, N. D., Hieronymus, H., Gopalan, A., Xiao, Y., Carver, B. S., Arora, V. K., Kaushik, P., Cerami, E. G., Reva, B. A., et al. (2010) · Cancer Cell · doi:10.1016/j.ccr.2010.05.026 · Cited by 3,713
Self-citationInternational network of cancer genome projects
The International Cancer Genome Consortium (2010) · Nature · doi:10.1038/nature08987 · Cited by 2,299
Predicting the functional impact of protein mutations: application to cancer genomics
Reva, B. A., Antipin, Y., & Sander, C. (2011) · Nucleic Acids Research · doi:10.1093/nar/gkr407 · Cited by 2,046
Self-citationHallmarks of 'BRCAness' in sporadic cancers
Turner, N. C., Tutt, A. N. J., & Ashworth, A. (2004) · Nature reviews. Cancer · doi:10.1038/nrc1457 · Cited by 1,690
Pathway Commons, a web resource for biological pathway data
Cerami, E. G., Gross, B. E., Demir, E., Rodchenkov, I., Babur, O., Anwar, N., Schultz, N., Bader, G. D., & Sander, C. (2011) · Nucleic Acids Research · doi:10.1093/nar/gkq1039 · Cited by 1,101
Self-citation
Research works printed but not linked: 1
- Cancer Genome Atlas Research Network, 2011, Nature, 474, 609, 10.1038/nature10166 · DOI · Paper page
Cited by
Sorted by citations
Items 901–1,000 of 1,118
JUNB governs a feed-forward network of TGFβ signaling that aggravates breast cancer invasion
Sundqvist, A., Morikawa, M., Ren, J., Vasilaki, E., Kawasaki, N., Kobayashi, M., Koinuma, D., Aburatani, H., Miyazono, K., Heldin, C., et al. (2017) · Nucleic Acids Research · doi:10.1093/nar/gkx1190 · Cited by 128
In silico cancer research towards 3R
Jean-Quartier, C., Jeanquartier, F., Jurišica, I., & Holzinger, A. (2018) · BMC Cancer · doi:10.1186/s12885-018-4302-0 · Cited by 132
The Ubiquitin Ligase TRIP12 Limits PARP1 Trapping and Constrains PARP Inhibitor Efficiency
Gatti, M., Imhof, R., Huang, Q. D., Baudis, M., & Altmeyer, M. (2020) · Cell Reports · doi:10.1016/j.celrep.2020.107985 · Cited by 135
Cytotoxic lymphocytes target characteristic biophysical vulnerabilities in cancer
Tello‐Lafoz, M., Srpan, K., Sanchez, E. E., Hu, J. Y., Remšík, J., Romin, Y., Calò, A., Hoen, D. R., Bhanot, U. K., Morris, L. G. T., et al. (2021) · Immunity · doi:10.1016/j.immuni.2021.02.020 · Cited by 129
Nonhistone Lysine Methylation in the Regulation of Cancer PathwaysPreprint
Carlson, S. M., & Gozani, O. (2016) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a026435 · Cited by 133
Barriga, F. M., Tsanov, K. M., Ho, Y.-J., Sohail, N., Zhang, A., Baslan, T., Wuest, A. N., Del Priore, I., Meškauskaitė, B., Livshits, G., et al. (2022) · Nature Cancer · doi:10.1038/s43018-022-00443-5 · Cited by 125
YAP activation protects urothelial cell carcinoma from treatment-induced DNA damage
Ciamporcero, E. S., Shen, H., Ramakrishnan, S., Ku, S., Chintala, S., Shen, L., Adelaiye-Ogala, R. M., Miles, K. M., Ullio, C., Pizzimenti, S., et al. (2015) · Oncogene · doi:10.1038/onc.2015.219 · Cited by 126
Barderas, R., Mendes, M. L., Torres, S., Bartolomé, R. A., López-Lucendo, M. F., Villar-Vázquez, R., Peláez‐García, A., Fuente, E., Bonilla, F., & Casal, J. I. (2013) · Molecular & Cellular Proteomics · doi:10.1074/mcp.m112.022848 · Cited by 126
Functional Roles of the E3 Ubiquitin Ligase UBR5 in Cancer
Shearer, R. F., Iconomou, M., Watts, C. K. W., & Saunders, D. N. (2015) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-15-0383 · Cited by 125
Defining actionable mutations for oncology therapeutic development
Carr, T. H., McEwen, R. K., Dougherty, B. A., Johnson, J. H., Dry, J. R., Lai, Z., Ghazoui, Z. F., Laing, N. M., Hodgson, D., Cruzalegui, F. H., et al. (2016) · Nature reviews. Cancer · doi:10.1038/nrc.2016.35 · Cited by 128
HGF/Met Signaling in Head and Neck Cancer: Impact on the Tumor Microenvironment
Hartmann, S., Bhola, N. E., & Grandis, J. R. (2016) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-16-0951 · Cited by 129
Rath, N., Morton, J. P., Julian, L., Helbig, L., Kadir, S. R., McGhee, E. J., Anderson, K. I., Kalna, G., Mullin, M., Pinho, A. V., et al. (2016) · EMBO Molecular Medicine · doi:10.15252/emmm.201606743 · Cited by 125
Albacker, L. A., Wu, J., Smith, P. G., Warmuth, M., Stephens, P. J., Zhu, P., Yu, L., & Chmielecki, J. (2017) · PLoS ONE · doi:10.1371/journal.pone.0176181 · Cited by 128
Tasks, Techniques, and Tools for Genomic Data Visualization
Nusrat, S., Harbig, T. A., & Gehlenborg, N. (2019) · Computer Graphics Forum · doi:10.1111/cgf.13727 · Cited by 141
Dissenting degradation: Deubiquitinases in cell cycle and cancer
Bonacci, T., & Emanuele, M. J. (2020) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2020.03.008 · Cited by 128
KIT and Melanoma: Biological Insights and Clinical Implications
Pham, D. D. M., Guhan, S. M., & Tsao, H. (2020) · Yonsei Medical Journal · doi:10.3349/ymj.2020.61.7.562 · Cited by 131
Tan, R. S. Y. C., Ong, W. S., Lee, K.-H., Lim, A. H., Park, S., Park, Y. H., Lin, C., Lu, Y., Ono, M., Ueno, T., et al. (2022) · BMC Medicine · doi:10.1186/s12916-022-02284-6 · Cited by 125
Oncogenes and tumor suppressor genes: functions and roles in cancers
Dakal, T. C., Dhabhai, B., Pant, A., Moar, K., Chaudhary, K., Yadav, V., Ranga, V., Sharma, N. K., Kumar, A., Maurya, P. K., et al. (2024) · MedComm · doi:10.1002/mco2.582 · Cited by 139
Dushyanthen, S., Teo, Z. L., Caramia, F., Savas, P., Mintoff, C. P., Virassamy, B., Henderson, M. A., Luen, S. J., Mansour, M., Kershaw, M. H., et al. (2017) · Nature Communications · doi:10.1038/s41467-017-00728-9 · Cited by 124
Haesen, D., Abbasi Asbagh, L., Derua, R., Hubert, A., Schrauwen, S., Hoorne, Y., Amant, F., Waelkens, E., Sablina, A., & Janssens, V. (2016) · Cancer Research · doi:10.1158/0008-5472.can-15-3342 · Cited by 124
The Architecture of the TIR Domain Signalosome in the Toll-like Receptor-4 Signaling Pathway
Guven‐Maiorov, E., Keskin, Ö., Gürsoy, A., Waes, C. V., Chen, Z., Tsai, C., & Nussinov, R. (2015) · Scientific Reports · doi:10.1038/srep13128 · Cited by 124
Khosravi‐Shahi, P., Cabezón‐Gutiérrez, L., & Custodio‐Cabello, S. (2017) · Asia-Pacific Journal of Clinical Oncology · doi:10.1111/ajco.12748 · Cited by 130
Kundu, S. T., Grzeskowiak, C. L., Fradette, J. J., Gibson, L. A., Rodriguez, L. B., Creighton, C. J., Scott, K. L., & Gibbons, D. L. (2018) · Nature Communications · doi:10.1038/s41467-018-05013-x · Cited by 124
Nami, B., & Wang, Z. (2018) · Cancers · doi:10.3390/cancers10080274 · Cited by 124
Zhuang, L., Yang, Z., & Meng, Z. (2018) · BioMed Research International · doi:10.1155/2018/7897346 · Cited by 124
RET rearrangements are actionable alterations in breast cancer
Paratala, B., Chung, J., Williams, C. B., Yilmazel, B., Petrosky, W., Williams, K. A., Schrock, A. B., Gay, L. M., Lee, E. C., Dolfi, S. C., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-07341-4 · Cited by 124
Frizzled-7 Is Required for Wnt Signaling in Gastric Tumors with and Without Apc Mutations
Flanagan, D. J., Barker, N., Costanzo, N. S. D., Mason, E. A., Gurney, A. L., Méniel, V. S., Koushyar, S., Austin, C. R., Ernst, M., Pearson, H. B., et al. (2019) · Cancer Research · doi:10.1158/0008-5472.can-18-2095 · Cited by 124
An Algorithmic Immunohistochemical Approach to Define Tumor Type and Assign Site of Origin
Bellizzi, A. M. (2020) · Advances in Anatomic Pathology · doi:10.1097/pap.0000000000000256 · Cited by 131
Wong, H. Y., Sheng, Q., Hesterberg, A. B., Croessmann, S., Rios, B. L., Giri, K. R., Jackson, J., Miranda, A. X., Watkins, E., Schaffer, K. R., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-33780-1 · Cited by 131
Epigenetic dysregulation from chromosomal transit in micronuclei
Agustinus, A. S., Al-Rawi, D. H., Dameracharla, B., Raviram, R., Jones, B. S. C. L., Stransky, S., Scipioni, L., Luebeck, J., Bona, M. D., Norkūnaitė, D., et al. (2023) · Nature · doi:10.1038/s41586-023-06084-7 · Cited by 130
Molecular Pathways: AXL, a Membrane Receptor Mediator of Resistance to Therapy
Scaltriti, M., Elkabets, M., & Baselga, J. M. (2016) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-15-1458 · Cited by 126
Synthetic lethality between the cohesin subunits STAG1 and STAG2 in diverse cancer contexts
van der Lelij, P., Lieb, S., Jude, J., Wutz, G., Santos, C. P., Falkenberg, K. J., Schlattl, A., Ban, J., Schwentner, R., Hoffmann, T., et al. (2017) · eLife · doi:10.7554/elife.26980 · Cited by 124
Zhang, X., Choi, P. S., Francis, J. M., Gao, G. F., Campbell, J. D., Ramachandran, A., Mitsuishi, Y., Ha, G., Shih, J., Vázquez, F., et al. (2017) · Cancer Discovery · doi:10.1158/2159-8290.cd-17-0532 · Cited by 126
Feng, X., Li, L., Wagner, E. J., & Li, W. (2017) · Nucleic Acids Research · doi:10.1093/nar/gkx892 · Cited by 123
Principe, D. R., Narbutis, M., Kumar, S., Park, A. J., Viswakarma, N., Dorman, M. J., Kamath, S. D., Grippo, P. J., Fishel, M. L., Hwang, R. F., et al. (2020) · Cancer Research · doi:10.1158/0008-5472.can-19-2959 · Cited by 130
The evolution of RET inhibitor resistance in RET-driven lung and thyroid cancers
Rosen, E. Y., Won, H. H., Zheng, Y., Cocco, E., Selçuklu, S. D., Gong, Y., Friedman, N. D., de Bruijn, I., Sümer, S. O., Bielski, C. M., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-28848-x · Cited by 123
Truncated FGFR2 is a clinically actionable oncogene in multiple cancers
Zingg, D., Bhin, J., Yemelyanenko, J., Kas, S. M., Rolfs, F., Lutz, C., Lee, J., Klarenbeek, S., Silverman, I. M., Annunziato, S., et al. (2022) · Nature · doi:10.1038/s41586-022-05066-5 · Cited by 124
Liu, Y., Sun, Y., Wang, P., Li, S., Dong, Y., Zhou, M., Shi, B., Jiang, H., Sun, R., & Li, Z. (2023) · Journal of Translational Medicine · doi:10.1186/s12967-023-04080-z · Cited by 128
Identification of an oncogenic RAB protein
Wheeler, D. B., Zoncu, R., Root, D. E., Sabatini, D. M., & Sawyers, C. L. (2015) · Science · doi:10.1126/science.aaa4903 · Cited by 125
ATM-Deficient Colorectal Cancer Cells Are Sensitive to the PARP Inhibitor Olaparib
Wang, C., Jette, N., Moussienko, D., Bebb, D. G., & Lees‐Miller, S. P. (2017) · Translational Oncology · doi:10.1016/j.tranon.2017.01.007 · Cited by 125
How Schwann cells facilitate cancer progression in nerves
Deborde, S., & Wong, R. J. (2017) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-017-2578-x · Cited by 122
Structure of human chromatin-remodelling PBAF complex bound to a nucleosome
Yuan, J., Chen, K., Zhang, W., & Chen, Z. (2022) · Nature · doi:10.1038/s41586-022-04658-5 · Cited by 122
Genomic landscape of pleural and peritoneal mesothelioma tumours
Hiltbrunner, S., Fleischmann, Z., Sokol, E. S., Zoche, M., Felley‐Bosco, E., & Fontecedro, A. C. (2022) · British Journal of Cancer · doi:10.1038/s41416-022-01979-0 · Cited by 125
Meng, X., Xiao, W., Sun, J., Li, W., Yuan, H., Yu, T., Zhang, X., & Dong, W. (2022) · Cancer Letters · doi:10.1016/j.canlet.2022.216023 · Cited by 126
Rare molecular subtypes of lung cancer
Harada, G., Yang, S., Cocco, E., & Drilon, A. E. D. C. (2023) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-023-00733-6 · Cited by 126
Quercetin regulates β-catenin signaling and reduces the migration of triple negative breast cancer
Srinivasan, A., Thangavel, C., Liu, Y., Shoyele, S., Den, R. B., Selvakumar, P., & Lakshmikuttyamma, A. (2015) · Molecular Carcinogenesis · doi:10.1002/mc.22318 · Cited by 123
Kundur, S., Prayag, A., Selvakumar, P., Nguyen, T., McKee, L., Cruz, C., Srinivasan, A., Shoyele, S., & Lakshmikuttyamma, A. (2018) · Journal of Cellular Physiology · doi:10.1002/jcp.27761 · Cited by 126
Vidovic, D., Huynh, T. T., Konda, P., Dean, C. A., Cruickshank, B. M., Sultan, M., Coyle, K. M., Gujar, S. A., & Marcato, P. (2019) · Cell Death and Differentiation · doi:10.1038/s41418-019-0362-1 · Cited by 121
Spitz melanoma is a distinct subset of spitzoid melanoma
Raghavan, S. S., Peternel, S., Mully, T. W., North, J. P., Pincus, L. B., LeBoit, P. E., McCalmont, T. H., Bastian, B. C., & Yeh, I. (2020) · Modern Pathology · doi:10.1038/s41379-019-0445-z · Cited by 125
Regulation of deoxynucleotide metabolism in cancer: novel mechanisms and therapeutic implications
Kohnken, R. A., Kodigepalli, K. M., & Wu, L. J. (2015) · Molecular Cancer · doi:10.1186/s12943-015-0446-6 · Cited by 128
Evolving Lessons on the Complex Role of AMPK in Normal Physiology and Cancer
Dasgupta, B., & Chhipa, R. R. (2015) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2015.11.007 · Cited by 121
Li, X., Wu, W. K. K., Xing, R., Wong, S. H., Liu, Y., Fang, X., Zhang, Y., Wang, M., Wang, J., Li, L., et al. (2016) · Cancer Research · doi:10.1158/0008-5472.can-15-2443 · Cited by 122
Herling, C., Klaumuenzer, M., Rocha, C. K., Altmüller, J., Thiele, H., Bahlo, J., Kluth, S., Crispatzu, G., Herling, M., Schiller, J., et al. (2016) · Blood · doi:10.1182/blood-2016-01-691550 · Cited by 123
Computational polypharmacology: a new paradigm for drug discovery
Chaudhari, R. R., Tan, Z., Huang, B., & Zhang, S. (2017) · Expert Opinion on Drug Discovery · doi:10.1080/17460441.2017.1280024 · Cited by 123
Shen, Q., Eun, J. W., Lee, K., Kim, H. S., Yang, H. D., Kim, S. Y., Lee, E. K., Kim, T., Kang, K., Kim, S., et al. (2017) · Hepatology · doi:10.1002/hep.29606 · Cited by 120
YAP and TAZ in Lung Cancer: Oncogenic Role and Clinical Targeting
Sardo, F. L., Strano, S., & Blandino, G. (2018) · Cancers · doi:10.3390/cancers10050137 · Cited by 124
KDM5B is a master regulator of the H3K4-methylome in stem cells, development and cancer
Xhabija, B., & Kidder, B. L. (2018) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2018.11.001 · Cited by 120
Deng, S.-J., Chen, H., Zeng, Z., Deng, S., Zhu, S., Zeng, Y., He, C., Liu, M., Huang, K., Zhong, J., et al. (2018) · Cancer Research · doi:10.1158/0008-5472.can-18-0419 · Cited by 120
Skvortsova, K., Masle‐Farquhar, E., Luu, P., Song, J. Z., Qu, W., Zotenko, E., Gould, C. M., Du, Q., Peters, T. J., Colino‐Sanguino, Y., et al. (2019) · Cancer Cell · doi:10.1016/j.ccell.2019.01.004 · Cited by 121
Ning, J.-F., Stanciu, M., Humphrey, M. R., Gorham, J., Wakimoto, H., Nishihara, R., Lees, J. A., Zou, L., Martuza, R. L., Wakimoto, H., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-10993-5 · Cited by 120
Nguyen, B., Mota, J. M., Nandakumar, S., Stopsack, K. H., Weg, E. S., Rathkopf, D. E., Morris, M. J., Scher, H. I., Kantoff, P. W., Gopalan, A., et al. (2020) · European Urology · doi:10.1016/j.eururo.2020.03.024 · Cited by 122
Self-citationMechanisms of Resistance to KRASG12C Inhibitors
Dunnett-Kane, V., Nicola, P. A., Blackhall, F. H., & Lindsay, C. R. (2021) · Cancers · doi:10.3390/cancers13010151 · Cited by 122
Mitochondrial dynamics regulate genome stability via control of caspase-dependent DNA damage
Cao, K., Riley, J. S., Heilig, R., Montes-Gómez, A. E., Vringer, E., Berthenet, K., Cloix, C., Elmasry, Y., Spiller, D. G., Ichim, G., et al. (2022) · Developmental Cell · doi:10.1016/j.devcel.2022.03.019 · Cited by 124
Tsang, Y. T. M., Deavers, M. T., Sun, C. C., Kwan, S., Kuo, E., Malpica, A. L., Mok, S. C., Gershenson, D. M., & Wong, K. (2013) · The Journal of Pathology · doi:10.1002/path.4252 · Cited by 119
Replicative DNA polymerase mutations in cancer
Heitzer, E., & Tomlinson, I. P. M. (2014) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2013.12.005 · Cited by 121
Onken, M. D., Winkler, A. E., Kanchi, K.-L., Chalivendra, V., Law, J. H., Rickert, C. G., Kallogjeri, D., Judd, N. P., Dunn, G. P., Piccirillo, J. F., et al. (2014) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-14-0205 · Cited by 119
RNF43 is a tumour suppressor gene mutated in mucinous tumours of the ovary
Ryland, G. L., Hunter, S. M., Doyle, M., Rowley, S. M., Christie, M., Allan, P. E., Bowtell, D. D. L., Chenevix‐Trench, G., Gorringe, K. L., & Campbell, I. (2012) · The Journal of Pathology · doi:10.1002/path.4134 · Cited by 126
Pan-Cancer Analysis of Mutation Hotspots in Protein Domains
Miller, M. L., Reznik, E., Gauthier, N. P., Aksoy, B. A., Korkut, A., Gao, J., Ciriello, G., Schultz, N. D., & Sander, C. (2015) · Cell Systems · doi:10.1016/j.cels.2015.08.014 · Cited by 121
Self-citationAGC1/2, the mitochondrial aspartate-glutamate carriers
Amoêdo, N. D., Punzi, G., Obre, É., Lacombe, D., Grassi, A., Pierri, C. L., & Rossignol, R. (2016) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2016.04.011 · Cited by 128
Mitochondrial dysfunction in cancer: Potential roles of ATF5 and the mitochondrial UPR
Deng, P., & Haynes, C. M. (2017) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2017.05.002 · Cited by 121
Tu, W. B., Shiah, Y.-J., Lourenco, C., Mullen, P. J., Dingar, D. D., Redel, C., Tamachi, A., Ba-Alawi, W., Aman, A. M., Al‐awar, R., et al. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.09.001 · Cited by 119
Stiff stroma increases breast cancer risk by inducing the oncogene ZNF217
Northey, J. J., Barrett, A. S., Acerbi, I., Hayward, M.-K., Talamantes, S., Dean, I. S., Mouw, J. K., Ponik, S. M., Lakins, J. N., Huang, P., et al. (2020) · Journal of Clinical Investigation · doi:10.1172/jci129249 · Cited by 119
Distinct Hodgkin lymphoma subtypes defined by noninvasive genomic profiling
Alig, S., Esfahani, M. S., Garofalo, A., Li, M. Y., Rossi, C., Flerlage, T., Flerlage, J. E., Adams, R., Binkley, M. S., Shukla, N., et al. (2023) · Nature · doi:10.1038/s41586-023-06903-x · Cited by 122
Broz, M. T., Ko, E. Y., Ishaya, K., Xiao, J.-F., Simone, M. C. D., Hoi, X. P., Piras, R., Gala, B., Tessaro, F. H. G., Karlstaedt, A., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-46504-4 · Cited by 123
Varghese, A. M., Perry, M., Chou, J. F., Nandakumar, S., Muldoon, D. M., Erakky, A., Zucker, A., Fong, C. J., Mehine, M. M., Nguyen, B., et al. (2025) · Nature Medicine · doi:10.1038/s41591-024-03362-3 · Cited by 122
Self-citationEvolution of metastasis revealed by mutational landscapes of chemically induced skin cancers
McCreery, M. Q., Halliwill, K. D., Chin, D., Delrosario, R., Hirst, G. L., Vuong, P. T., Jen, K., Hewinson, J., Adams, D. J., & Balmain, A. (2015) · Nature Medicine · doi:10.1038/nm.3979 · Cited by 119
Blessing, A. M., Rajapakshe, K., Bollu, L. R., Shi, Y., White, M. A., Pham, A. H., Lin, C., Jonsson, P., Cortés, C. J., Cheung, E. C. W., et al. (2016) · Autophagy · doi:10.1080/15548627.2016.1268300 · Cited by 120
Walsh, L. A., Alvarez, M. J., Sabio, E. Y., Reyngold, M., Makarov, V., Mukherjee, S., Lee, K.-W., Desrichard, A., Turcan, Ş., Dalin, M. G., et al. (2017) · Cell Reports · doi:10.1016/j.celrep.2017.07.052 · Cited by 118
Bclaf1 promotes angiogenesis by regulating HIF-1α transcription in hepatocellular carcinoma
Wen, Y., Zhou, X., Lu, M., He, M., Tian, Y., Liu, L., Wang, M., Tan, W., Deng, Y., Yang, X., et al. (2018) · Oncogene · doi:10.1038/s41388-018-0552-1 · Cited by 118
Li, B., Zhang, B., Wang, X., Zeng, Z., Huang, Z., Zhang, L., Wei, F., Ren, X., & Yang, L. (2020) · OncoImmunology · doi:10.1080/2162402x.2020.1807291 · Cited by 118
Kriegsman, B. A., Vangala, P., Chen, B. J., Meraner, P., Brass, A. L., Garber, M., & Rock, K. L. (2019) · The Journal of Immunology · doi:10.4049/jimmunol.1900475 · Cited by 114
RNA-binding proteins, multifaceted translational regulators in cancer
Wurth, L., & Gebauer, F. (2014) · Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms · doi:10.1016/j.bbagrm.2014.10.001 · Cited by 121
Dave, B., Granados-Principal, S. M., Zhu, R., Benz, S. C., Rabizadeh, S., Soon‐Shiong, P., Yu, K., Shao, Z., Li, X., Gilcrease, M. Z., et al. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1320769111 · Cited by 122
SerpinB2 regulates stromal remodelling and local invasion in pancreatic cancer
Initiative, A. P. C. G., Harris, N. L. E., Vennin, C., Conway, J. R. W., Vine, K. L., Pinese, M., Cowley, M. J., Shearer, R. F., Lucas, M. C., Herrmann, D., et al. (2017) · Oncogene · doi:10.1038/onc.2017.63 · Cited by 121
Pal, S. K., Ali, S. M., Yakirevich, E., Geynisman, D. M., Karam, J. A., Elvin, J. A., Frampton, G. M., Huang, X., Lin, D. I., Rosenzweig, M. R., et al. (2017) · European Urology · doi:10.1016/j.eururo.2017.05.033 · Cited by 119
Zhang, T., Zhou, J., Zhang, W., Lin, J., Ma, J., Wen, X., Yuan, Q., Li, X., Xu, Z., & Qian, J. (2018) · Clinical Epigenetics · doi:10.1186/s13148-018-0486-z · Cited by 117
Zhao, Y., Pan, Z., Namburi, S., Pattison, A., Posner, A., Balachander, S., Paisie, C. A., Reddi, H. V., Rueter, J., Gill, A. J., et al. (2020) · EBioMedicine · doi:10.1016/j.ebiom.2020.103030 · Cited by 120
The bone microenvironment increases phenotypic plasticity of ER+ breast cancer cells
Bado, I., Zhang, W., Hu, J., Xu, Z., Wang, H., Sarkar, P., Li, L., Wan, Y., Liu, J., Wu, W., et al. (2021) · Developmental Cell · doi:10.1016/j.devcel.2021.03.008 · Cited by 120
Cyclin E1 and RTK/RAS signaling drive CDK inhibitor resistance via activation of E2F and ETS
Taylor‐Harding, B., Aspuria, P.-J. P., Agadjanian, H., Cheon, D., Mizuno, T., Greenberg, D. N., Allen, J. R., Spurka, L., Funari, V. A., Spiteri, E., et al. (2014) · Oncotarget · doi:10.18632/oncotarget.2673 · Cited by 117
SIRT2 activates G6PD to enhance NADPH production and promote leukaemia cell proliferation
Xu, S., Wang, T.-S., Li, X., & Wang, Y.-P. (2016) · Scientific Reports · doi:10.1038/srep32734 · Cited by 117
Sridhara, S. R. C., Carvalho, S., Grosso, A. R., Gallego-Paez, L. M., Carmo‐Fonseca, M., & de Almeida, S. F. (2017) · Cell Reports · doi:10.1016/j.celrep.2016.12.050 · Cited by 116
Recurrent IDH2 R172X mutations in sinonasal undifferentiated carcinoma
Jo, V. Y., Chau, N. G., Hornick, J. L., Krane, J. F., & Sholl, L. M. (2017) · Modern Pathology · doi:10.1038/modpathol.2016.239 · Cited by 116
Hajek, M., Sewell, A. B., Kaech, S. M., Burtness, B. A., Yarbrough, W. G., & Issaeva, N. (2017) · Cancer · doi:10.1002/cncr.30570 · Cited by 116
Cholesterol uptake and regulation in high-grade and lethal prostate cancers
Stopsack, K. H., Gerke, T. A., Andrén, O., Andersson, S., Giovannucci, E. L., Mucci, L. A., & Rider, J. R. (2017) · Carcinogenesis · doi:10.1093/carcin/bgx058 · Cited by 116
Karunanithi, S., Levi, L., DeVecchio, J., Karagkounis, G., Reizes, O., Lathia, J. D., Kalady, M. F., & Noy, N. (2017) · Stem Cell Reports · doi:10.1016/j.stemcr.2017.06.002 · Cited by 117
Patel, K., van der Vos, K. E., Smith, C. G., Mouliere, F. C., Tsui, D. W. Y., Morris, J., Chandrananda, D., Marass, F., van den Broek, D. A., Neal, D. E., et al. (2017) · Scientific Reports · doi:10.1038/s41598-017-05623-3 · Cited by 117
Lung adenocarcinoma: from molecular basis to genome-guided therapy and immunotherapy
Chalela, R., Curull, V., Enríquez-Rodríguez, C. J., Pijuán, L., Bellosillo, B., & Gea, J. (2017) · Journal of Thoracic Disease · doi:10.21037/jtd.2017.06.20 · Cited by 119
Imperial, R. J. L., Ahmed, Z., Toor, O. M., Erdoğan, C., Khaliq, A. M., Case, P., Case, J., Kennedy, K. F., Cummings, L. S., Melton, N. M., et al. (2018) · Molecular Cancer · doi:10.1186/s12943-018-0923-9 · Cited by 121
Vilgelm, A. E., Pawlikowski, J. S., Liu, Y., Hawkins, O. E., Davis, T. A., Smith, J., Weller, K. P., Horton, L. W., McClain, C. M., Ayers, G. D., et al. (2015) · Cancer Research · doi:10.1158/0008-5472.can-14-2405 · Cited by 115
Shia, J., Schultz, N., Kuk, D., Vakiani, E., Middha, S., Segal, N. H., Hechtman, J. F., Berger, M. F., Stadler, Z. K., Weiser, M. R., et al. (2017) · Modern Pathology · doi:10.1038/modpathol.2016.198 · Cited by 105
Self-citation
Metadata
- Authors
- Cerami, E., Gao, J., Dogrusoz, U., Gross, B. E., Sumer, S. O., Aksoy, B. A., Jacobsen, A., Byrne, C. J., Heuer, M. L., Larsson, E., Antipin, Y., Reva, B., Goldberg, A. P., Sander, C., & Schultz, N.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Authors' Affiliations: 1Computational Biology Center, Memorial Sloan-Kettering Cancer Center, 2Tri-Institutional Training Program in Computational Biology and Medicine, New York, New York; and 3Computer Engineering Department, Bilkent University, Ankara, Turkey
- Corresponding author
- Cerami, Ethan
- ORCID
- Venue
- Cancer Discovery
- Published
- 2012-05-01
- Volume
- 2
- Issue
- 5
- Pages
- 401-404
- ISSN
- 2159-8274 (ISSN-L)
- 2159-8290
- PMC
- PMC3956037
- OpenAlex
- W2149441684
- Semantic Scholar
- b8d2639696825d163188eb5cea5582c350987b70
- Cited by
- 17,455
- References
- 17
- Citations by year
- 2026: 945 · 2025: 1525 · 2024: 1764 · 2023: 2020 · 2022: 2020 · 2021: 2136 · 2020: 1836 · 2019: 1393 · 2018: 1048 · 2017: 906 · 2016: 764 · 2015: 583 · 2014: 324 · 2013: 159 · 2012: 15
- FWCI
- 114.79
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cancer Discovery (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Bilkent University Institutional Repository (Bilkent University) (submittedVersion, other-oa)
- Bilkent University Institutional Repository (Bilkent University) (submittedVersion)
- Funders
- Memorial Sloan-Kettering Cancer Center
- University of Toronto
- Bilkent Üniversitesi
- National Institutes of Health
- University of Texas MD Anderson Cancer Center
- Stand Up To Cancer (SU2C‐AACR‐DT0209)
- National Cancer Institute (SU2C-AACR-DT0209, R01CA132744, U24CA143840, NCI-U24CA143840, NCI-R21CA135870, R21CA135870)
- National Institute of General Medical Sciences (GM 103504, P41GM103504)
- National Center for Research Resources (RR031228, P41RR031228)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bioinformatics and Genomic Networks
- Keywords
- cancer genomics data, interactive data exploration, tumor molecular profiles, clinical features, cancer research resources
- MeSH terms
- Database Management Systems, Humans, Neoplasms, Databases, Factual, Internet, Genomics
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 ›
Are you an author, or do you see a problem with this page? Request a review
