ArticleNature2014
Rb suppresses human cone-precursor-derived retinoblastoma tumours.
Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
127 citing papers in PubMed, 1 synthesis or guideline pooled it, 234 citations in OpenAlex.
- A Meta-Analysis of Retinoblastoma Copy Numbers Refines the List of Possible Driver Genes Involved in Tumor Progression.PloS one · 2016Pooled it
- Why are Some Tissues More Vulnerable? Revisiting Tissue Specificity in Hereditary Cancer Syndromes.Molecular diagnosis & therapy · 2026Review
- A tumor-associated photoreceptor signature unifies distinct central nervous system malignancies.Cancer cell · 2026Article
- BCOR Mutations Deregulate Cell Cycle and Hypoxic Adaptation Pathways in Retinoblastoma.Molecular cancer research : MCR · 2026Article
- Longitudinal analysis of retinal cell state transitions in RB1-deficient retinal organoids reveals the nascent cone precursors are the earliest cell-origin of human retinoblastoma.Cell death & disease · 2026Article
- High-throughput screening of drug libraries identifies a new synergistic drug combination for the treatment of retinoblastoma.PloS one · 2026Article
- Post-translational modifications in retinoblastoma: mechanisms, immune regulation, and therapeutic opportunities.Frontiers in immunology · 2026Review
- NSUN2 contributes to the RB malignant progression and Glycolysis by mediating the m5C methylation modification of HKDC1.Journal of bioenergetics and biomembranes · 2025Article
- Human Retinal Organoid Modeling Defines Developmental Window and Therapeutic Vulnerabilities in MYCN-Amplified Retinoblastoma.International journal of molecular sciences · 2025Article
- Genetics of Retinoblastoma: An Overview and Significance of Genetic Testing in Clinical Practice.Genes · 2025Review
- Article
- Comprehensive analysis of disulfidoptosis-related genes reveals molecular heterogeneity and key regulators in retinoblastoma progression.Translational pediatrics · 2025Article
- Retinoma: An overview.Pediatric investigation · 2025Review
- Article
- Delving Into Retinoblastoma Genetics: Discovery of Novel Mutations and Their Clinical Impact: Retrospective Cohort Study.Cancer medicine · 2025Article
- Tumor heterogeneity in retinoblastoma: a literature review.Cancer metastasis reviews · 2025Review
- Bringing p53 Back: A Prion-Powered Attack on Retinoblastoma.International journal of biological sciences · 2025Article
- PDGFR-α shRNA-polyplex for uveal melanoma treatment via EMT mediated vasculogenic mimicry interfering.Journal of nanobiotechnology · 2024Article
- Phenotypic Biomarkers of Aqueous Extracellular Vesicles from Retinoblastoma Eyes.International journal of molecular sciences · 2024Article
- Minimal Requirements for Cancer Initiation: A Comparative Consideration of Three Prototypes of Human Leukemia.Cancers · 2024Review
67 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Retinoblastoma is a childhood retinal tumour that initiates in response to biallelic RB1 inactivation and loss of functional retinoblastoma (Rb) protein. Although Rb has diverse tumour-suppressor functions and is inactivated in many cancers, germline RB1 mutations predispose to retinoblastoma far more strongly than to other malignancies. This tropism suggests that retinal cell-type-specific circuitry sensitizes to Rb loss, yet the nature of the circuitry and the cell type in which it operates have been unclear. Here we show that post-mitotic human cone precursors are uniquely sensitive to Rb depletion. Rb knockdown induced cone precursor proliferation in prospectively isolated populations and in intact retina. Proliferation followed the induction of E2F-regulated genes, and depended on factors having strong expression in maturing cone precursors and crucial roles in retinoblastoma cell proliferation, including MYCN and MDM2. Proliferation of Rb-depleted cones and retinoblastoma cells also depended on the Rb-related protein p107, SKP2, and a p27 downregulation associated with cone precursor maturation. Moreover, Rb-depleted cone precursors formed tumours in orthotopic xenografts with histological features and protein expression typical of human retinoblastoma. These findings provide a compelling molecular rationale for a cone precursor origin of retinoblastoma. More generally, they demonstrate that cell-type-specific circuitry can collaborate with an initiating oncogenic mutation to enable tumorigenesis.
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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.