ArticleOncogenesis2018
Double agents: genes with both oncogenic and tumor-suppressor functions.
Article in Oncogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
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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.
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Who cites it
77 citing papers in PubMed, 133 citations in OpenAlex.
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- Comparative analysis and correlation of cancer hotspot proteins and cell markers in tumor-normal adjacent breast and kidney samples using RPPA and LC-MS.Scientific reports · 2026Article
- Targeting thymidylate synthase enhances CD8 + T-cell infiltration and inhibits tumor growth in cervical cancer.Medical oncology (Northwood, London, England) · 2026Article
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- Evaluating the Antitumor Potential of Cannabichromene, Cannabigerol, and Related Compounds fromInternational journal of molecular sciences · 2025Article
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- Non-Viral RNA Therapies for Non-Small Cell Lung Cancer and Their Corresponding Clinical Trials.Molecular pharmaceutics · 2025Review
- Revealing cancer driver genes through integrative transcriptomic and epigenomic analyses with Moonlight.PLoS computational biology · 2025Article
- Sociobiology meets oncology: unraveling altruistic cooperation in cancer cells and its implications.Experimental & molecular medicine · 2025Review
- Prognostic and tumor microenvironmental features of gastric cancer revealed by macrophage polarization and protein lactylation-related genes.Frontiers in genetics · 2025Article
- Advances in predicting breast cancer driver mutations: Tools for precision oncology (Review).International journal of molecular medicine · 2025Review
- Re-evaluation of the relationship between PrPc expression and patient prognosis in primary esophageal squamous cell carcinoma and primary hepatocellular carcinoma.Scientific reports · 2024Article
- CancerPro: deciphering the pan-cancer prognostic landscape through combinatorial enrichment analysis and knowledge network insights.NAR genomics and bioinformatics · 2024Article
- In silico RNA isoform screening to identify potential cancer driver exons with therapeutic applications.Nature communications · 2024Article
- Copy number losses of oncogenes and gains of tumor suppressor genes generate common driver mutations.Nature communications · 2024Article
17 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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of genetic components in cancer development is an area of interest for cancer biologists in general. Intriguingly, some genes have both oncogenic and tumor-suppressor functions. In this study, we systematically identified these genes through database search and text mining. We find that most of them are transcription factors or kinases and exhibit dual biological functions, e.g., that they both positively and negatively regulate transcription in cells. Some cancer types such as leukemia are over-represented by them, whereas some common cancer types such as lung cancer are under-represented by them. Across 12 major cancer types, while their genomic mutation patterns are similar to that of oncogenes, their expression patterns are more similar to that of tumor-suppressor genes. Their expression profile in six human organs propose that they mainly function as tumor suppressor in normal tissue. Our network analyses further show they have higher network degrees than both oncogenes and tumor-suppressor genes and thus tend to be the hub genes in the protein-protein interaction network. Our mutation, expression spectrum, and network analyses might help explain why some cancer types are specifically associated with them. Finally, our results suggest that the functionally altering mutations in "double-agent" genes and oncogenes are the main driving force in cancer development, because non-silent mutations are biasedly distributed toward these two gene sets across all 12 major cancer types.
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.