ReviewCells2020
Tumor Suppressors Having Oncogenic Functions: The Double Agents.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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
52 citing papers in PubMed, 95 citations in OpenAlex.
- BMAL1 silencing as a promising chemosensitizing strategy for triple-negative breast cancer.Acta pharmacologica Sinica · 2026Article
- mRNA-based therapeutics in lung Cancer: Mechanisms, applications, and translational challenges.Journal, genetic engineering & biotechnology · 2026Review
- Transcription factors remodel tumor immune microenvironment by impacting multiple immune cells.Discover oncology · 2026Review
- 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
- The Janus Face of SPAG6: Inducing EMT in Luminal Breast Cancer Cells Amidst Widespread Expression Loss in Breast Tumours.Journal of cellular and molecular medicine · 2025Article
- Claspin and Cancer: Where Are We Now?International journal of molecular sciences · 2025Review
- The DEAD-box RNA helicase DDX28 suppresses cell migration and 3D growth and invasion in MDA-MB-231 cells by altering bioenergetics.Molecular biology of the cell · 2025Article
- Review
- Oncogenic properties of wild-type DNA repair gene FANCA in breast cancer.Cell reports · 2025Article
- Revealing cancer driver genes through integrative transcriptomic and epigenomic analyses with Moonlight.PLoS computational biology · 2025Article
- Review
- Amyloids in bladder cancer hijack cancer-related proteins and are positive correlated to tumor stage.Scientific reports · 2025Article
- The interplay of p16INK4a and non-coding RNAs: bridging cellular senescence, aging, and cancer.Biogerontology · 2025Review
- Sociobiology meets oncology: unraveling altruistic cooperation in cancer cells and its implications.Experimental & molecular medicine · 2025Review
- Immunotherapy in Glioblastoma: An Overview of Current Status.Clinical pharmacology : advances and applications · 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
- Integrated analysis of cell cycle and p53 signaling pathways related genes in breast, colorectal, lung, and pancreatic cancers: implications for prognosis and drug sensitivity for therapeutic potential.Discover oncology · 2024Article
- Article
- Article
- CIBRA identifies genomic alterations with a system-wide impact on tumor biology.Bioinformatics (Oxford, England) · 2024Article
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
No grant is acknowledged in the PubMed record.
Abstract
Cancer progression involves multiple genetic and epigenetic events, which involve gain-of-functions of oncogenes and loss-of-functions of tumor suppressor genes. Classical tumor suppressor genes are recessive in nature, anti-proliferative, and frequently found inactivated or mutated in cancers. However, extensive research over the last few years have elucidated that certain tumor suppressor genes do not conform to these standard definitions and might act as "double agents", playing contrasting roles in vivo in cells, where either due to haploinsufficiency, epigenetic hypermethylation, or due to involvement with multiple genetic and oncogenic events, they play an enhanced proliferative role and facilitate the pathogenesis of cancer. This review discusses and highlights some of these exceptions; the genetic events, cellular contexts, and mechanisms by which four important tumor suppressors-pRb, PTEN, FOXO, and PML display their oncogenic potentials and pro-survival traits in cancer.
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.