ArticleCancer cell2010
Dissecting the unique role of the retinoblastoma tumor suppressor during cellular senescence.
Article in Cancer cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 245 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
245 citing papers in PubMed, 1 synthesis or guideline pooled it, 378 citations in OpenAlex.
- Integration of TP53, DREAM, MMB-FOXM1 and RB-E2F target gene analyses identifies cell cycle gene regulatory networks.Nucleic acids research · 2016Pooled it
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- A conserved regulatory architecture stabilizes cellular senescence across distinct triggers in human fibroblasts.GeroScience · 2026Article
- Lipopolysaccharide stimulates dynamic changes in B cell metabolism to promote proliferation.eLife · 2026Article
- Review
- The role of circular RNAs in mediating the protective effects of exercise against muscle degeneration and aging.Biogerontology · 2026Review
- Article
- The roles of cell cycle proteins in regulating the tumor immune microenvironment.Genes & diseases · 2026Review
- BRCA1 and BRCA2 gene expression: p53- and cell cycle-dependent repression requires RB and DREAM.Cell death and differentiation · 2026Article
- A CDK4/6 inhibitor-armed oncolytic adenovirus reverses T cell exhaustion through the Rb-p65-CCL5 pathway and potentiates the antitumor activity of anti-PD-1 or CAR-T therapy in colorectal cancer.Frontiers in immunology · 2026Article
- A narrative review of therapy-induced senescence in cancer: mechanisms, immune interplay, and therapeutic opportunities.Journal of the Egyptian National Cancer Institute · 2025Review
- Activation of AKT1 enhances the capacity of senescent BMSCs to regulate osteoclast activation.Molecular medicine reports · 2025Article
- Determination of ADP/ATP translocase isoform ratios in malignancy and cellular senescence.Molecular oncology · 2025Article
- JMJD3-mediated senescence is required to overcome stress-induced hematopoietic defects.EMBO reports · 2025Article
- A transcriptome-based human universal senescence index (hUSI) robustly predicts cellular senescence under various conditions.Nature aging · 2025Article
- Potentiating doxorubicin activity through BCL-2 inhibition in p53 wild-type and mutated triple-negative breast cancer.Frontiers in oncology · 2025Article
- The impact of cellular senescence on aging skeletal muscle.Frontiers in cell and developmental biology · 2025Review
- A Boolean model explains phenotypic plasticity changes underlying hepatic cancer stem cells emergence.NPJ systems biology and applications · 2024Article
- Article
185 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
The RB protein family (RB, p107, and p130) has overlapping and compensatory functions in cell-cycle control. However, cancer-associated mutations are almost exclusively found in RB, implying that RB has a nonredundant role in tumor suppression. We demonstrate that RB preferentially associates with E2F target genes involved in DNA replication and is uniquely required to repress these genes during senescence but not other growth states. Consequently, RB loss leads to inappropriate DNA synthesis following a senescence trigger and, together with disruption of a p21-mediated cell-cycle checkpoint, enables extensive proliferation and rampant genomic instability. Our results identify a nonredundant RB effector function that may contribute to tumor suppression and reveal how loss of RB and p53 cooperate to bypass senescence.
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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.