Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (694 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Genes whose gain-of-function alterations lead to neoplastic cell transformation. They include, for example, genes for activators or stimulators of cell proliferation such as growth factors, growth factor receptors, protein kinases, signal transducers, nuclear phosphoproteins, and transcription factors. A prefix of v- before oncogene symbols indicates oncogenes captured and transmitted by retroviruses; the prefix c- before the gene symbol of an oncogene indicates it is the cellular homolog (proto-oncogenes) of a v-oncogene.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Oncogene; Transforming Gene; Genes, Transforming; Gene, Transforming; Transforming Genes.
Where it fits in the MeSH classification
- Broader topics
- Genes, Neoplasm
- Narrower topics
- Proto-Oncogenes
Related concepts
- Neoplastic Cell Transformation
- Cell Proliferation
- Retroviruses
- Proto-Oncogenes
Research landscape
PubMed indexes 58,494 records tagged with the MeSH heading “Oncogenes” (counts retrieved 2026-10-29). 4,113 of them (7.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 28,795 records.
Reviews account for 9,966 records (17.0%) and meta-analyses for 108. Randomized controlled trials number 174 (0.3%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 28,795 |
| 2000-2009 | 15,438 |
| 2010-2019 | 10,148 |
| 2020 onward | 4,113 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 9,966 | 17.0% |
| Meta-analyses | 108 | 0.2% |
| Randomized controlled trials | 174 | 0.3% |
Method: PubMed query "Oncogenes"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in genetics and genomics
Genetic findings vary widely in strength. A variant linked to a condition in one study may not replicate in other ancestries, and most common variants have small effects that are meaningful only in aggregate. Studies of rare, high-impact variants can support strong causal claims about a gene, while association studies describe statistical links that need functional and independent replication. Check the sample size, the ancestry of participants, whether results were replicated, and whether a laboratory or clinical outcome was actually measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Role of oncogenic KRAS in the prognosis, diagnosis and treatment of colorectal cancer | 2021 | Review article Design not recorded in structured metadata | 422 | cc by PMID 34742312 · DOI · PMC8571891 |
| The evolutionary dynamics of extrachromosomal DNA in human cancers | 2022 | Research article Design not recorded in structured metadata | 216 | cc by PMID 36123406 · DOI · PMC9534767 |
| Origins and impact of extrachromosomal DNA | 2024 | Research article Design not recorded in structured metadata | 183 | cc by PMID 39506150 · DOI · PMC11540846 |
| Mechanisms of enhancer-driven oncogene activation | 2026 | Review article Design not recorded in structured metadata | 4 | cc by PMID 39853740 · DOI · PMC12628035 |
Role of oncogenic KRAS in the prognosis, diagnosis and treatment of colorectal cancer [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Colorectal cancer (CRC) is a heterogeneous disease at the cellular and molecular levels.
- Closing excerpt
- Here, we provide an overview of the role of KRAS in the prognosis, diagnosis and treatment of CRC.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (163 words)
Colorectal cancer (CRC) is a heterogeneous disease at the cellular and molecular levels. Kirsten rat sarcoma (KRAS) is a commonly mutated oncogene in CRC, with mutations in approximately 40% of all CRC cases; its mutations result in constitutive activation of the KRAS protein, which acts as a molecular switch to persistently stimulate downstream signaling pathways, including cell proliferation and survival, thereby leading to tumorigenesis. Patients whose CRC harbors KRAS mutations have a dismal prognosis. Currently, KRAS mutation testing is a routine clinical practice before treating metastatic cases, and the approaches developed to detect KRAS mutations have exhibited favorable sensitivity and accuracy. Due to the presence of KRAS mutations, this group of CRC patients requires more precise therapies. However, KRAS was historically thought to be an undruggable target until the development of KRASG12C allele-specific inhibitors. These promising inhibitors may provide novel strategies to treat KRAS-mutant CRC. Here, we provide an overview of the role of KRAS in the prognosis, diagnosis and treatment of CRC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34742312 · DOI · PMC8571891
The evolutionary dynamics of extrachromosomal DNA in human cancers [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Oncogene amplification on extrachromosomal DNA (ecDNA) is a common event, driving aggressive tumor growth, drug resistance and shorter survival.
- Closing excerpt
- These results show how the nonchromosomal random inheritance pattern of ecDNA contributes to poor outcomes for patients with cancer.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (157 words)
Oncogene amplification on extrachromosomal DNA (ecDNA) is a common event, driving aggressive tumor growth, drug resistance and shorter survival. Currently, the impact of nonchromosomal oncogene inheritance-random identity by descent-is poorly understood. Also unclear is the impact of ecDNA on somatic variation and selection. Here integrating theoretical models of random segregation, unbiased image analysis, CRISPR-based ecDNA tagging with live-cell imaging and CRISPR-C, we demonstrate that random ecDNA inheritance results in extensive intratumoral ecDNA copy number heterogeneity and rapid adaptation to metabolic stress and targeted treatment. Observed ecDNAs benefit host cell survival or growth and can change within a single cell cycle. ecDNA inheritance can predict, a priori, some of the aggressive features of ecDNA-containing cancers. These properties are facilitated by the ability of ecDNA to rapidly adapt genomes in a way that is not possible through chromosomal oncogene amplification. These results show how the nonchromosomal random inheritance pattern of ecDNA contributes to poor outcomes for patients with cancer.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36123406 · DOI · PMC9534767
Origins and impact of extrachromosomal DNA [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Extrachromosomal DNA (ecDNA) is a major contributor to treatment resistance and poor outcome for patients with cancer1,2.
- Closing excerpt
- These results shed light on why ecDNA is a substantial clinical problem that can cooperatively drive tumour growth signals, alter transcriptional landscapes and suppress the immune system.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (229 words)
Extrachromosomal DNA (ecDNA) is a major contributor to treatment resistance and poor outcome for patients with cancer1,2. Here we examine the diversity of ecDNA elements across cancer, revealing the associated tissue, genetic and mutational contexts. By analysing data from 14,778 patients with 39 tumour types from the 100,000 Genomes Project, we demonstrate that 17.1% of tumour samples contain ecDNA. We reveal a pattern highly indicative of tissue-context-based selection for ecDNAs, linking their genomic content to their tissue of origin. We show that not only is ecDNA a mechanism for amplification of driver oncogenes, but it also a mechanism that frequently amplifies immunomodulatory and inflammatory genes, such as those that modulate lymphocyte-mediated immunity and immune effector processes. Moreover, ecDNAs carrying immunomodulatory genes are associated with reduced tumour T cell infiltration. We identify ecDNAs bearing only enhancers, promoters and lncRNA elements, suggesting the combinatorial power of interactions between ecDNAs in trans. We also identify intrinsic and environmental mutational processes linked to ecDNA, including those linked to its formation, such as tobacco exposure, and progression, such as homologous recombination repair deficiency. Clinically, ecDNA detection was associated with tumour stage, more prevalent after targeted therapy and cytotoxic treatments, and associated with metastases and shorter overall survival. These results shed light on why ecDNA is a substantial clinical problem that can cooperatively drive tumour growth signals, alter transcriptional landscapes and suppress the immune system.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39506150 · DOI · PMC11540846
Mechanisms of enhancer-driven oncogene activation [4]
Abstract reading summary — source excerpts
- Opening excerpt
- An aggressive subtype of acute myeloid leukemia (AML) is caused by enhancer hijacking resulting in MECOM overexpression.
- Closing excerpt
- Gaining mechanistic insight in both enhancer deregulation and super-enhancer activity is critical to pave the way for new treatments for AML and other cancers that are the result of enhancer deregulation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (145 words)
An aggressive subtype of acute myeloid leukemia (AML) is caused by enhancer hijacking resulting in MECOM overexpression. Several chromosomal rearrangements can lead to this: the most common (inv(3)/t(3;3)) results in a hijacked GATA2 enhancer, and there are several atypical MECOM rearrangements involving enhancers from other hematopoietic genes. The set of enhancers which can be hijacked by MECOM can also be hijacked by BCL11B. Enhancer deregulation is also a driver of oncogenesis in a range of other malignancies. The mechanisms of enhancer deregulation observed in other cancer types, including TAD boundary disruptions and the creation of de novo (super-) enhancers, may explain overexpression of MECOM or other oncogenes in AML without enhancer hijacking upon translocation. Gaining mechanistic insight in both enhancer deregulation and super-enhancer activity is critical to pave the way for new treatments for AML and other cancers that are the result of enhancer deregulation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39853740 · DOI · PMC12628035
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Epigenetic plasticity and the hallmarks of cancer [5]
- Research article A compendium of mutational cancer driver genes [6]
- Research article The MYC oncogene - the grand orchestrator of cancer growth and immune evasion [7]
- Research article Mutant p53 as a guardian of the cancer cell [8]
- Research article Targeted Therapies for Lung Cancer Patients With Oncogenic Driver Molecular Alterations [9]
- Research article OncomiR or Tumor Suppressor? The Duplicity of MicroRNAs in Cancer [10]
References
- Zhu G, Pei L, Xia H, Tang Q, Bi F. Role of oncogenic KRAS in the prognosis, diagnosis and treatment of colorectal cancer. . 2021. PMID 34742312 · DOI · PMC8571891
- Lange JT, Rose JC, Chen CY, Pichugin Y, Xie L, Tang J, et al.. The evolutionary dynamics of extrachromosomal DNA in human cancers. . 2022. PMID 36123406 · DOI · PMC9534767
- Bailey C, Pich O, Thol K, Watkins TBK, Luebeck J, Rowan A, et al.. Origins and impact of extrachromosomal DNA. . 2024. PMID 39506150 · DOI · PMC11540846
- Vriend J, Delwel R, Pastoors D. Mechanisms of enhancer-driven oncogene activation. . 2026. PMID 39853740 · DOI · PMC12628035
- Flavahan WA, Gaskell E, Bernstein BE. Epigenetic plasticity and the hallmarks of cancer. Science. 2017. PMID 28729483 · DOI · PMC5940341
- Martínez-Jiménez F, Muiños F, Sentís I, Deu-Pons J, Reyes-Salazar I, Arnedo-Pac C, et al.. A compendium of mutational cancer driver genes. Nat Rev Cancer. 2020. PMID 32778778 · DOI
- Dhanasekaran R, Deutzmann A, Mahauad-Fernandez WD, Hansen AS, Gouw AM, Felsher DW. The MYC oncogene - the grand orchestrator of cancer growth and immune evasion. Nat Rev Clin Oncol. 2022. PMID 34508258 · DOI · PMC9083341
- Mantovani F, Collavin L, Del Sal G. Mutant p53 as a guardian of the cancer cell. Cell Death Differ. 2019. PMID 30538286 · DOI · PMC6329812
- Tan AC, Tan DSW. Targeted Therapies for Lung Cancer Patients With Oncogenic Driver Molecular Alterations. J Clin Oncol. 2022. PMID 34985916 · DOI
- Svoronos AA, Engelman DM, Slack FJ. OncomiR or Tumor Suppressor? The Duplicity of MicroRNAs in Cancer. Cancer Res. 2016. PMID 27325641 · DOI · PMC4930690
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.