ArticleGenes & development2004
Tissue-specific tumor suppressor activity of retinoblastoma gene homologs p107 and p130.
Article in Genes & development, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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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.
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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.
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Who cites it
83 citing papers in PubMed, 138 citations in OpenAlex.
- Why are Some Tissues More Vulnerable? Revisiting Tissue Specificity in Hereditary Cancer Syndromes.Molecular diagnosis & therapy · 2026Review
- Genetically Modified Mouse Models for Sarcoma Research: A Comprehensive Review.Current oncology reports · 2025Review
- The Tumor Suppressor p53 Downregulates p107 (International journal of molecular sciences · 2025Article
- Human Retinal Organoid Modeling Defines Developmental Window and Therapeutic Vulnerabilities in MYCN-Amplified Retinoblastoma.International journal of molecular sciences · 2025Article
- Article
- Analysis of pathogenic variants in retinoblastoma reveals a potential gain of function mutation.Genes & cancer · 2025Article
- Histone Deacetylases in Retinoblastoma.International journal of molecular sciences · 2024Review
- Patterns in the tapestry of chromatin-bound RB.Trends in cell biology · 2024Review
- Monitoring the Cell Cycle of Tumor Cells in Mouse Models of Human Cancer.Cold Spring Harbor perspectives in medicine · 2023Article
- RB1-deficient prostate tumor growth and metastasis are vulnerable to ferroptosis induction via the E2F/ACSL4 axis.The Journal of clinical investigation · 2023Article
- Retinoblastoma Protein Paralogs and Tumor Suppression.Frontiers in genetics · 2022Review
- Article
- The Role and Clinical Implications of the Retinoblastoma (RB)-E2F Pathway in Gastric Cancer.Frontiers in oncology · 2021Review
- Review
- Retinoblastoma: Etiology, Modeling, and Treatment.Cancers · 2020Review
- Single-Cell Analysis of Human Retina Identifies Evolutionarily Conserved and Species-Specific Mechanisms Controlling Development.Developmental cell · 2020Article
- RBL1 (p107) functions as tumor suppressor in glioblastoma and small-cell pancreatic neuroendocrine carcinoma in Xenopus tropicalis.Oncogene · 2020Article
- Identification of microRNA-mRNA regulatory networks and pathways related to retinoblastoma across human and mouse.International journal of ophthalmology · 2020Article
- Low dose ionizing radiation strongly stimulates insertional mutagenesis in a γH2AX dependent manner.PLoS genetics · 2020Article
- Loss of p53 suppresses replication-stress-induced DNA breakage in G1/S checkpoint deficient cells.eLife · 2018Article
23 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
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The retinoblastoma gene family consists of three genes: RB, p107, and p130. While loss of pRB causes retinoblastoma in humans and pituitary gland tumors in mice, tumorigenesis in other tissues may be suppressed by p107 and p130. To test this hypothesis, we have generated chimeric mice from embryonic stem cells carrying compound loss-of-function mutations in the Rb gene family. We found that Rb/p107- and Rb/p130-deficient mice were highly cancer prone. We conclude that in a variety of tissues tumor development by loss of pRB is suppressed by its homologs p107 and p130. The redundancy of the retinoblastoma proteins in vivo is reflected by the behavior of Rb-family-defective mouse embryonic fibroblasts in vitro.
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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.