ReviewAnnals of translational medicine2016
Determining the incidence of the hereditary form of retinoblastoma.
Review in Annals of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Clinical characteristics, treatment and prognosis of infants with retinoblastoma: a multicenter, 10-year retrospective analysis.BMC pediatrics · 2023Article
- Long Non-coding RNA FEZF1-AS1 Promotes Growth and Reduces Apoptosis Through Regulation of miR-363-3p/PAX6 Axis in Retinoblastoma.Biochemical genetics · 2021Article
- The National Registry of Retinoblastoma in Japan (1983-2014).Japanese journal of ophthalmology · 2018Article
- miR-145 regulates the proliferation and apoptosis of Y79 human retinoblastoma cells by targeting IGF-1R.International journal of clinical and experimental pathology · 2018Article
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
No grant is acknowledged in the PubMed record.
Abstract
Retinoblastoma (Rb) is used here as the prototype of a condition which has a dominant mode of inheritance. Under the two-hit model of carcinogenesis, a germinal mutation may be followed by somatic mutation producing a tumour or tumours, in which case the carrier has relatively lower fitness. If somatic mutation does not occur, the carrier is assumed to have normal fitness, that is the Rb germinal mutation is incompletely penetrant. Formulae are given for the frequency of the Rb allele and the incidence of Rb in equilibrium as functions of the mutation rate, penetrance and fitness.
Indexed as
Identifiers
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.