Evidence map›Paper›PMID 22203015›Full record

ArticleLangenbeck's archives of surgery2012

Clinical impact of TP53 alterations in adrenocortical carcinomas.

Jens Waldmann, Nikolaos Patsalis, Volker Fendrich, Peter Langer, Wolfgang Saeger, Brunhilde Chaloupka, Annette Ramaswamy, Martin Fassnacht, Detlef K Bartsch, Emily P Slater

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Langenbeck's archives of surgery, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

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  14. The role of microRNAs in the adrenocortical carcinomas.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  15. Article
  16. Development of adrenal cortex zonation.Endocrinology and metabolism clinics of North America · 2015
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Jens WaldmannDepartment of Visceral, Thoracic and Vascular Surgery, University Hospital Giessen and Marburg, Baldingerstraße, 35043, Marburg, Germany. jwaldman@med.uni-marburg.de
Nikolaos Patsalis
Volker Fendrich
Peter Langer
Wolfgang Saeger
Brunhilde Chaloupka
Annette Ramaswamy
Martin Fassnacht
Detlef K Bartsch
Emily P Slater
Universitätsklinikum Gießen und Marburg · DEMarienkrankenhaus Hamburg · DEUniversitätsklinikum Würzburg · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTo evaluate the role of somatic TP53 mutations and to correlate somatic and germline mutations with results of immunostaining, a large cohort of ACC patients was analyzed. PATIENTS AND

methodsPatients with ACC who underwent potential curative surgery at the authors' department were screened for TP53 somatic and germline mutations in exons 5, 6, 7, 8, and 10 by DHPLC analysis. Aberrant samples were further analyzed by direct sequencing. Immunostaining was performed on corresponding paraffin sections in all patients. Complete clinical and follow-up data were correlated with the status of TP53.

resultsThirty ACC patients were included. Four of 30 patients showed aberrant DHPLC configuration and direct sequencing confirmed 2 (7%) germline mutations (R337H, R248W), 1 (3%) somatic mutation (R213X), and 1 (3%) noncoding polymorphism (g.17708 A>T). The only patient with a positive family history harbored a TP53 mutation. Tumors of the three patients with mutations showed aberrant p53 expression in more than 10% of cells by immunostaining, compared to only 3 of 27 patients without mutations (p = 0.009). Aberrant p53 expression (>5%) was detected in 12/30 (40%) ACCs. The latter was associated with an increased Ki67 and van Slooten index (p ≤ 0.001; p = 0.020). Disease-free survival decreased significantly in patients with aberrant p53 IHC of more than 5% of cells (65.7 ± 12.4 vs. 26.6 ± 8.7 months; p = 0.043 log rank test).

conclusionsPatients with ACC revealed aberrant expression of p53 in 40%, and mutations were identified in 25% of these patients. Therefore aberrant p53 expression should be considered an indicator for genetic testing. A subgroup of apparently sporadic ACC is caused by TP53 germline mutations, and family history is a strong indicator for p53 germline mutations.

Indexed as

Germ-Line MutationAdolescentAdrenal Cortex NeoplasmsAdrenalectomyAdrenocortical CarcinomaAdultAgedCohort StudiesDisease-Free SurvivalDNA-Binding ProteinsDNA Mutational AnalysisFemaleGene Expression Regulation, NeoplasticGenes, p53Genetic TestingHumansDNA-Binding ProteinsTP53TG1 protein, human

Identifiers

PMID22203015
OpenAlexW2026906603

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.