ArticleJournal of neuro-oncology2019
Age-dependent copy number variations of TP53 tumour suppressor gene associated with altered phosphorylation status of p53 protein in sporadic schwannomas.
Article in Journal of neuro-oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed, 0 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
purposePoint mutations of TP53 tumour suppressor are very rare in schwannomas. We aim to characterize the frequency of exonic copy-number changes of the gene in the tumour and to examine the association between TP53 alterations, phosphorylation status of p53 protein and clinical phenotypes.
methodsThe alterations of TP53 were screened by a combination of Sanger sequencing and multiplex ligation-dependent probe amplification (MLPA) in a total of 44 vestibular schwannomas. The mutation index (MI) in a tumour was defined as the number of exons mutated/ the number of exons tested. Phosphorylation status of p53 protein was investigated by immunoblotting and immunofluorescence.
resultsMLPA analysis showed single and multi-exon deletion mutations of TP53 in 65.7% of the cases. Comparisons of clinical features between mutated and non-mutated patients established an association of TP53 mutations with progressive phenotypes, including an earlier formation and a larger tumour. In addition, there were significant correlations between MI and both patients' age and tumour size. The Ser 392 phosphorylation level of p53 varied among tumours, and correlation analysis revealed an age-dependent phosphorylation pattern. The majority of tumours with hyperphosphorylated p53 were from mutated and young patients, suggesting an association of Ser392 phosphorylation with the mutational status of TP53 involved in the acceleration of tumour growth in young individuals. Moreover, Ser 392 phosphorylation contributed to a nuclear accumulation of p53 in schwannona cultures with TP53 mutation.
conclusionsAn interplay between the mutation status of TP53, phosphorylation patterns and tumour behaviors might be established in the disease.
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.