ArticleOncogene2002
Tumor formation in mice with somatic inactivation of the retinoblastoma gene in interphotoreceptor retinol binding protein-expressing cells.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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.
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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
35 citing papers in PubMed, 72 citations in OpenAlex.
- An imbalance between proliferation and differentiation underlies the development of microRNA-defective pineoblastoma.Genes & development · 2025Article
- Drosha: a new tumor suppressor in pineoblastoma.Genes & development · 2025Article
- Article
- Genetics and current research models of Mendelian tumor predisposition syndromes with ocular involvement.Progress in retinal and eye research · 2025Review
- Recent Advances in Pineoblastoma Research: Molecular Classification, Modelling and Targetable Vulnerabilities.Cancers · 2025Review
- Retinoblastoma: Etiology, Modeling, and Treatment.Cancers · 2020Review
- Modeling germline mutations in pineoblastoma uncovers lysosome disruption-based therapy.Nature communications · 2020Article
- Developmental stage-specific proliferation and retinoblastoma genesis in RB-deficient human but not mouse cone precursors.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Structural changes of the macula and optic nerve head in the remaining eyes after enucleation for retinoblastoma: an optical coherence tomography study.BMC ophthalmology · 2017Article
- Transgenic Models in Retinoblastoma Research.Ocular oncology and pathology · 2015Review
- Inactivation of Rb and E2f8 synergizes to trigger stressed DNA replication during erythroid terminal differentiation.Molecular and cellular biology · 2014Article
- Animal models in retinoblastoma research.Saudi journal of ophthalmology : official journal of the Saudi Ophthalmological Society · 2013Article
- Retinal horizontal cells lacking Rb1 sustain persistent DNA damage and survive as polyploid giant cells.Molecular biology of the cell · 2012Article
- Concomitant inactivation of Rb and E2f8 in hematopoietic stem cells synergizes to induce severe anemia.Blood · 2012Article
- Article
- Nuclear factor I/B is an oncogene in small cell lung cancer.Genes & development · 2011Article
- Article
- Rescue of myogenic defects in Rb-deficient cells by inhibition of autophagy or by hypoxia-induced glycolytic shift.The Journal of cell biology · 2010Article
- Retinal pigment epithelium defects accelerate photoreceptor degeneration in cell type-specific knockout mouse models of choroideremia.Investigative ophthalmology & visual science · 2010Article
- Rb deletion in mouse mammary progenitors induces luminal-B or basal-like/EMT tumor subtypes depending on p53 status.The Journal of clinical investigation · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The retinoblastoma suppressor gene product Rb has been assigned a critical role in cell cycle regulation, the induction of differentiation, and inhibition of oncogenic transformation. Inheritance of a mutant RB allele in humans is responsible for bilateral retinoblastoma, a malignant tumor of the retina. Trilateral retinoblastoma (TRB) is a rare variant of familial retinoblastoma in which, in addition to retinal tumors, tumors develop from the pineal gland, an organ ontologically related to the retina. Germline inactivation of Rb in mice leads to mid-gestational lethality with defects in erythropoeisis and neurogenesis. This embryonic lethality prohibits the analysis of Rb function in selected cell types at later stages of development or in the adult. Here, we describe the Cre-LoxP mediated somatic inactivation of Rb in a subset of neuroendocrine cells, including photoreceptor cells. We observed neuroendocrine tumors of the pineal and pituitary gland. These tumors invariably showed inactivation of Rb and Trp53. Remarkably, loss of Rb in photoreceptor cells does not lead to retinoblastoma or any phenotypic changes, not even when photoreceptor cells are made deficient in Rb, p107 and Trp53. Our results highlight the important differences that exist in tumor susceptibility between mice and man (e.g pineal gland) and question the photoreceptor cell origin of human retinoblastoma.
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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.