ReviewGenes & development2016
RB1: a prototype tumor suppressor and an enigma.
Review in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 278 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
278 citing papers in PubMed, 421 citations in OpenAlex.
- Trial
- Article
- Large-scale Genomic Landscape and Clinical Outcomes of De Novo and Treatment-emergent Neuroendocrine Prostate Cancer.European urology open science · 2026Article
- Histone Variant H2A.Z2 Hyper-Transcription Induced by E2F1 Accelerates Lung Adenocarcinoma Progression via the JAK-STAT Signaling Pathway.Thoracic cancer · 2026Article
- Genome-Wide DNA Methylation Profiling Reveals Ancestry-Associated Epigenetic Reprogramming in Cervical Intraepithelial Neoplasia.International journal of molecular sciences · 2026Article
- Variant allele frequency as a potential marker in response to frontline systemic therapy for patients with locally advanced and metastatic urothelial carcinoma.Translational andrology and urology · 2026Article
- CRISPR Interference to Inhibit Oncogenes for Cancer Therapy.International journal of molecular sciences · 2026Review
- Is cancer the result of uncontrolled cellular growth? a glance into the tumorigenic process.Cancer cell international · 2026Review
- Unraveling syndrome-driven osteosarcoma: genetic insights and therapeutic frontiers.Orphanet journal of rare diseases · 2026Review
- Association between elevated PRIM1 expression and poor prognosis in human urothelial carcinoma.Journal of Taibah University Medical Sciences · 2026Article
- Separate transcription and splicing gene networks are linked and coordinated by the pRb-E2F pathway.Nucleic acids research · 2026Article
- i-motifs: DNA structures with regulatory functions and therapeutic potential.Einstein (Sao Paulo, Brazil) · 2026Review
- BRCA1 and BRCA2 gene expression: p53- and cell cycle-dependent repression requires RB and DREAM.Cell death and differentiation · 2026Article
- New understanding of the molecular pathogenesis and therapeutic progress of hepatocellular carcinoma.Oncology reviews · 2026Review
- Subtype-Dependent Transcriptional Coupling Between DNMT1 and E2F-Linked Proliferative Programs in Breast Cancer: A Dual-Cohort Transcriptomic Analysis.Journal of Cancer · 2026Article
- Modeling the Effects of Single Nucleotide Polymorphisms (SNPs) on the Structure and Function of the HumanHuman mutation · 2026Article
- Article
- Article
- Monod: model-based discovery and integration through fitting stochastic transcriptional dynamics to single-cell sequencing data.Nature methods · 2025Article
- A novel soil Bacillus strain GB_SG_008: isolation, characterization, and anticancer potential of an intracellular protein fraction inducing apoptosis and modulating cancer marker proteins.Archives of microbiology · 2025Article
218 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 susceptibility gene (RB1) was the first tumor suppressor gene to be molecularly defined. RB1 mutations occur in almost all familial and sporadic forms of retinoblastoma, and this gene is mutated at variable frequencies in a variety of other human cancers. Because of its early discovery, the recessive nature of RB1 mutations, and its frequency of inactivation, RB1 is often described as a prototype for the class of tumor suppressor genes. Its gene product (pRB) regulates transcription and is a negative regulator of cell proliferation. Although these general features are well established, a precise description of pRB's mechanism of action has remained elusive. Indeed, in many regards, pRB remains an enigma. This review summarizes some recent developments in pRB research and focuses on progress toward answers for the three fundamental questions that sit at the heart of the pRB literature: What does pRB do? How does the inactivation of RB change the cell? How can our knowledge of RB function be exploited to provide better treatment for cancer patients?
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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 Socratic graph.