SynthesisCancer research2013
Cooperation and antagonism among cancer genes: the renal cancer paradigm.
Synthesis in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- New developments in existing WHO entities and evolving molecular concepts: The Genitourinary Pathology Society (GUPS) update on renal neoplasia.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Guideline
- Molecular Genetic Determinants of Shorter Time on Active Surveillance in a Prospective Phase 2 Clinical Trial in Metastatic Renal Cell Carcinoma.European urology · 2022Trial
- Expression of PBRM1 as a prognostic predictor in metastatic renal cell carcinoma patients treated with tyrosine kinase inhibitor.International journal of clinical oncology · 2020Trial
- Molecular underpinnings of metastatic small renal masses.JCI insight · 2026Article
- Stimulator of interferon genes (STING) in renal tumors: Biological bases, diagnostic relevance, and predictive potential.Histology and histopathology · 2026Review
- SETD2 methyltransferase activity promotes correct transcription initiation and termination.EMBO reports · 2026Article
- Determinants of pancreatic tropism in metastatic renal cell carcinoma.JCI insight · 2026Article
- Review
- Article
- APOC2 Promotes Clear Cell Renal Cell Carcinoma Progression via Activation of the JAK-STAT Signaling Pathway.Current issues in molecular biology · 2025Article
- Determinants of late metastases in renal cell carcinoma.Journal of the National Cancer Institute · 2025Article
- Revealing the characteristics of SETD2-mutated clear cell renal cell carcinoma through tumor heterogeneity analysis.Frontiers in genetics · 2024Article
- Genomic Profiling and Molecular Characterization of Clear Cell Renal Cell Carcinoma.Current oncology (Toronto, Ont.) · 2023Review
- Epigenetic and transcriptomic characterization reveals progression markers and essential pathways in clear cell renal cell carcinoma.Nature communications · 2023Article
- The expanding role of BAP1 in clear cell renal cell carcinoma.Human pathology · 2023Review
- Primary and acquired resistance to first-line therapy for clear cell renal cell carcinoma.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- Exosomes in Genitourinary Cancers: Emerging Mediators of Drug Resistance and Promising Biomarkers.International journal of biological sciences · 2023Review
- Predicting Oncologic Outcomes in Small Renal Tumors.European urology oncology · 2022Article
- 2022 WUOF/SIU International Consultation on Urological Diseases: Genetics and Tumor Microenvironment of Renal Cell Carcinoma.Societe internationale d'urologie journal : SIUJ · 2022Article
- Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
It is poorly understood how driver mutations in cancer genes work together to promote tumor development. Renal cell carcinoma (RCC) offers a unique opportunity to study complex relationships among cancer genes. The four most commonly mutated genes in RCC of clear-cell type (the most common type) are two-hit tumor suppressor genes, and they cluster in a 43-Mb region on chromosome 3p that is deleted in approximately 90% of tumors: VHL (mutated in ∼80%), PBRM1 (∼50%), BAP1 (∼15%), and SETD2 (∼15%). Meta-analyses that we conducted show that mutations in PBRM1 and SETD2 co-occur in tumors at a frequency higher than expected by chance alone, indicating that these mutations may cooperate in tumorigenesis. In contrast, consistent with our previous results, mutations in PBRM1 and BAP1 tend to be mutually exclusive. Mutation exclusivity analyses (often confounded by lack of statistical power) raise the possibility of functional redundancy. However, mutation exclusivity may indicate negative genetic interactions, as proposed herein for PBRM1 and BAP1, and mutations in these genes define RCC with different pathologic features, gene expression profiles, and outcomes. Negative genetic interactions among cancer genes point toward broader context dependencies of cancer gene action beyond tissue dependencies. An enhanced understanding of cancer gene dependencies may help to unravel vulnerabilities that can be exploited therapeutically.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.