ReviewOncogene2015
Antitumor mechanisms when pRb and p53 are genetically inactivated.
Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 48 citations in OpenAlex.
- Kinase Plasticity with Vandetanib Treatment Enhances Sensitivity to Tamoxifen in Estrogen Receptor Positive Breast Cancer.Molecular cancer therapeutics · 2026Article
- Review
- Review
- Oxidative stress and antioxidants in breast cancer: a double-edged sword.Frontiers in oncology · 2026Review
- The Role of Hepatic SIRT1: From Metabolic Regulation to Immune Modulation and Multi-target Therapeutic Strategies.Journal of clinical and translational hepatology · 2025Review
- Thyroid C-Cell Biology and Oncogenic Transformation.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2025Review
- Genetic and Epigenetic Interactions Involved in Senescence of Stem Cells.International journal of molecular sciences · 2024Review
- IDH1 mutation produces R-2-hydroxyglutarate (R-2HG) and induces mir-182-5p expression to regulate cell cycle and tumor formation in glioma.Biological research · 2024Article
- Identification and validation of an E2F-related gene signature for predicting recurrence-free survival in human prostate cancer.Cancer cell international · 2022Article
- Targeting the untargetable: RB1-deficient tumours are vulnerable to Skp2 ubiquitin ligase inhibition.British journal of cancer · 2022Review
- Integration of Adverse Outcome Pathways, Causal Networks and 'Omics to Support Chemical Hazard Assessment.Frontiers in toxicology · 2022Article
- The Biological and Biomechanical Role of Transglutaminase-2 in the Tumour Microenvironment.Cancers · 2021Review
- The Function of SUMOylation and Its Role in the Development of Cancer Cells under Stress Conditions: A Systematic Review.Stem cells international · 2020Review
- Glucose Transporter 1 Promotes the Malignant Phenotype of Non-Small Cell Lung Cancer through Integrin β1/Src/FAK Signaling.Journal of Cancer · 2019Article
- The silencing of long non-coding RNA ANRIL suppresses invasion, and promotes apoptosis of retinoblastoma cells through the ATM-E2F1 signaling pathway.Bioscience reports · 2018Article
- FGF9/FGFR2 increase cell proliferation by activating ERK1/2, Rb/E2F1, and cell cycle pathways in mouse Leydig tumor cells.Cancer science · 2018Article
- Genomic structure, expression, and functional characterization of checkpoint kinase 1 from Penaeus monodon.PloS one · 2018Article
- Aryl hydrocarbon receptor regulates histone deacetylase 8 expression to repress tumor suppressive activity in hepatocellular carcinoma.Oncotarget · 2017Article
- Effects of concomitant inactivation of p53 and pRb on response to doxorubicin treatment in breast cancer cell lines.Cell death discovery · 2017Article
- Role of CDKN2C Copy Number in Sporadic Medullary Thyroid Carcinoma.Thyroid : official journal of the American Thyroid Association · 2016Article
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 1 institution in 1 country.
Funding
Abstract
pRb and p53 are the two major tumor suppressors. Their inactivation is frequent when cancers develop and their reactivation is rationale of most cancer therapeutics. When pRb and p53 are genetically inactivated, cells irreparably lose the antitumor mechanisms afforded by them. Cancer genome studies document recurrent genetic inactivation of RB1 and TP53, and the inactivation becomes more frequent in more advanced cancers. These findings may explain why more advanced cancers are more likely to resist current therapies. Finding successful treatments for more advanced and multi-therapy-resistant cancers will depend on finding antitumor mechanisms that remain effective when pRb and p53 are genetically inactivated. Here, we review studies that have begun to make progress in this direction.
Indexed as
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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.