Evidence map›Paper›PMID 24590827›Full record

ArticleJournal of neuro-oncology2014

TP53 and p53 statuses and their clinical impact in diffuse low grade gliomas.

Emeline Gillet, Agusti Alentorn, Brahima Doukouré, Emeline Mundwiller, Hinke F van Thuijl, Hinke van Thuij, Jaap C Reijneveld, José Alfonso Meza Medina, Amélie Liou, Yannick Marie and 5 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Journal of neuro-oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.

  1. Molecular Biomarker Testing for the Diagnosis of Diffuse Gliomas.Archives of pathology & laboratory medicine · 2022
    Guideline
  2. Pooled it
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  13. Association ofBioMed research international · 2022
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  16. Cancers · 2021
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4 · The record

Corrections and comments

  • Erratum issued
    Van Thuij, Hinke [corrected to van Thuijl, Hinke F]
5 · Who and what money

Authors and funding

15 authors at 6 institutions in 2 countries.

Emeline GilletCentre de Recherche de l'Institut du Cerveau et de la Moelle Epinière (CRICM), Université Pierre et Marie Curie-Paris 6, UMRS 975, Paris, France.
Agusti Alentorn
Brahima Doukouré
Emeline Mundwiller
Hinke F van Thuijl
Hinke van Thuij
Jaap C Reijneveld
José Alfonso Meza Medina
Amélie Liou
Yannick Marie
Karima Mokhtari
Khê Hoang-Xuan
Marc Sanson
Jean-Yves Delattre
Ahmed Idbaih
Sorbonne Université · FRInstitut du Cerveau · FRAmsterdam UMC Location VUmc · NLInserm · FRAssistance Publique – Hôpitaux de Paris · FRPitié-Salpêtrière Hospital · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TP53 is a pivotal gene frequently mutated in diffuse gliomas and particularly in astrocytic tumors. The majority of studies dedicated to TP53 in gliomas were focused on mutational hotspots located in exons 5-8. Recent studies have suggested that TP53 is also mutated outside the classic mutational hotspots reported in gliomas. Therefore, we have sequenced all TP53 coding exons in a retrospective series of 61 low grade gliomas (LGG) using high throughput sequencing technology. In addition, TP53 mutational status was correlated with: (i) p53 expression, (ii) tumor type, (iii) chromosome arms 1p/19q status and (iv) clinical features of patients. The cohort included 32 oligodendrogliomas (O), 21 oligoastrocytomas (M) and 8 astrocytomas (A). TP53 mutation was detected in 52.4% (32/61) of tumors (34% of O, 71.4% of M and 75% of A). All mutations (38 mutations in 32 samples) were detected in exons 4, 5, 6, 7, 8 and 10. Missense and non-missense mutations, including seven novel mutations, were detected in 42.6 and 9.8% of tumors respectively. TP53 mutations were almost mutually exclusive with 1p/19q co-deletion and were associated with: (i) astrocytic phenotype, (ii) younger age, (iii) p53 expression. Using a threshold of 10% p53-positive tumor cells, p53 expression is an interesting surrogate marker for missense TP53 mutations (Se = 92%; Sp = 79.4%) but not for non-missense mutation (18.4% of mutations). TP53 and p53 statuses were not prognostic in LGG. In conclusion, we have identified novel TP53 mutations in LGG. TP53 mutations outside exons 4-8 are rare. Although it remains imperfect, p53 expression with a threshold of 10% is a good surrogate marker for missense TP53 mutations and appears helpful in the setting of LGG phenotype diagnosis.

Indexed as

AdultBrain NeoplasmsChromosomes, Human, Pair 19ExonsFemaleGliomaHumansMaleMiddle AgedMutationRetrospective StudiesROC CurveSurvival AnalysisTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID24590827
OpenAlexW2023114647

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.