ReviewOncogene2006
pRb2/p130: a new candidate for retinoblastoma tumor formation.
Review in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 24 citations in OpenAlex.
- Retinoblastoma: An update on genetic origin, classification, conventional to next-generation treatment strategies.Heliyon · 2024Review
- Preclinical evaluation of CDK4 phosphorylation predicts high sensitivity of pleural mesotheliomas to CDK4/6 inhibition.Molecular oncology · 2024Article
- RBL2/p130 is a direct AKT target and is required to induce apoptosis upon AKT inhibition in lung cancer and mesothelioma cell lines.Oncogene · 2018Article
- Mutational screening of germlineMolecular vision · 2018Article
- Proteomic profiling of retinoblastoma by high resolution mass spectrometry.Clinical proteomics · 2016Article
- Orchestrating epigenetic roles targeting ocular tumors.OncoTargets and therapy · 2016Review
- Gene expression profiling identifies different sub-types of retinoblastoma.British journal of cancer · 2013Article
- Analysis of retinoblastoma age incidence data using a fully stochastic cancer model.International journal of cancer · 2012Article
- Molecular biology of retinoblastoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2008Review
- Medulloblastoma: from molecular pathology to therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinoblastoma is the most common primary intraocular tumor in childhood. Mutations in both the alleles of the RB1 gene represent the causative agent for the tumor to occur. It is becoming evident that, although these alterations represent key events in the genesis of retinoblastoma, they are not sufficient per se for the tumor to develop, and other additional genetic or epigenetic alterations must occur. A supportive role in the genesis of retinoblastoma has recently been proposed for the RB1-related gene RB2/p130. Additionally, several other genetic alterations involving different chromosomes have been described as relevant in the tumorigenic process. In this review we will analyse current knowledge about the molecular mechanisms involved in retinoblastoma, paying particular attention to the mechanisms of inactivation of the biological function of the retinoblastoma family of proteins.
Indexed as
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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.