ReviewOncogene2006
The retinoblastoma tumor-suppressor gene, the exception that proves the rule.
Review in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
82 citing papers in PubMed, 164 citations in OpenAlex.
- Trial
- AI-driven CRISPR strategies in breast cancer: Organoid modeling, adaptive editing, and precision delivery.Iranian journal of basic medical sciences · 2026Review
- Cell Cycle Plasticity and Heterogeneity: An Underappreciated Feature of Cancer and Treatment Response.Cancer heterogeneity and plasticity · 2025Article
- Developmental cues are encoded by the combinatorial phosphorylation of Arabidopsis RETINOBLASTOMA-RELATED protein RBR1.The EMBO journal · 2024Article
- Review
- The role of aberrant DNA methylation in cancer initiation and clinical impacts.Therapeutic advances in medical oncology · 2024Article
- Review
- Seeing is believing: the impact of RB on nuclear organization.Cell cycle (Georgetown, Tex.) · 2023Article
- Retinoblastoma protein as an intrinsic BRD4 inhibitor modulates small molecule BET inhibitor sensitivity in cancer.Nature communications · 2022Article
- Cancer cell cycle dystopia: heterogeneity, plasticity, and therapy.Trends in cancer · 2022Review
- Active RB causes visible changes in nuclear organization.The Journal of cell biology · 2022Article
- Retinoblastoma Protein Paralogs and Tumor Suppression.Frontiers in genetics · 2022Review
- Regulatory genes in the androgen production, uptake and conversion (APUC) pathway in advanced prostate cancer.Endocrine oncology (Bristol, England) · 2022Review
- Changes in gene-gene interactions associated with cancer onset and progression are largely independent of changes in gene expression.iScience · 2021Article
- Article
- In-Vitro Anticancer and Antioxidant Activities of Eremina desertorum (Forsskal, 1775) Snail Mucin.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- The OncogeneCancers · 2021Article
- Human papillomavirus in retinoblastoma: A tertiary eye care center study from South India.Indian journal of ophthalmology · 2021Article
- A Hepatocellular Carcinoma Patient withVisceral medicine · 2021Article
- Overview of CaExploration of targeted anti-tumor therapy · 2021Review
22 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
1 author at 1 institution in 1 country.
Funding
Abstract
The retinoblastoma tumor-suppressor gene (Rb1) is centrally important in cancer research. Mutational inactivation of Rb1 causes the pediatric cancer retinoblastoma, while deregulation of the pathway in which it functions is common in most types of human cancer. The Rb1-encoded protein (pRb) is well known as a general cell cycle regulator, and this activity is critical for pRb-mediated tumor suppression. The main focus of this review, however, is on more recent evidence demonstrating the existence of additional, cell type-specific pRb functions in cellular differentiation and survival. These additional functions are relevant to carcinogenesis suggesting that the net effect of Rb1 loss on the behavior of resulting tumors is highly dependent on biological context. The molecular mechanisms underlying pRb functions are based on the cellular proteins it interacts with and the functional consequences of those interactions. Better insight into pRb-mediated tumor suppression and clinical exploitation of pRb as a therapeutic target will require a global view of the complex, interdependent network of pocket protein complexes that function simultaneously within given tissues.
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.