Evidence map›Paper›PMID 37295554›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2023

Recurrent Tumor Suppressor Alterations in Primary Pericardial Mesothelioma.

Inga-Marie Schaefer, Adrian Mariño-Enríquez, Mark M Hammer, Robert F Padera, Lynette M Sholl

Open access · bronzeAbstract read
In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.1field-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

6 citing papers in PubMed, 8 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Inga-Marie SchaeferDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. Electronic address: ischaefer@bwh.harvard.edu.
Adrian Mariño-EnríquezDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Mark M HammerDepartment of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Robert F PaderaDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Lynette M ShollDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Brigham and Women's Hospital · US

Funding

Targeting cell cycle dysregulation in GISTK08CA241085 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI SCHAEFER, INGA-MARIE · 2019 to 2023
$1.5M
NCI NIH HHS K08 CA241085
6 · The paper itself

Abstract

Primary pericardial mesotheliomas are extremely rare, accounting for <1% of all mesotheliomas, and their molecular genetic features and predisposing factors remain to be determined. Here, we report the clinicopathologic, immunohistochemical, and molecular genetic findings of 3 pericardial mesotheliomas without pleural involvement. Three cases diagnosed between 2004 and 2022 were included in the study and analyzed by immunohistochemistry and targeted next-generation sequencing (NGS); corresponding nonneoplastic tissue was sequenced in all cases. Two patients were female and 1 was male, aged between 66 and 75 years. Two patients each had prior asbestos exposure and were smokers. Histologic subtypes were epithelioid in 2 cases and biphasic in 1 case. Immunohistochemical staining identified expression of cytokeratin AE1/AE3 and calretinin in all cases, D2-40 in 2 cases, and WT1 in 1 case. Staining for tumor suppressors revealed loss of p16, MTAP, and Merlin (NF2) expression in 2 cases and loss of BAP1 and p53 in 1 case. Abnormal cytoplasmic BAP1 expression was observed in an additional case. Protein expression abnormalities correlated with NGS results, which showed concurrent complete genomic inactivation of CDKN2A/p16, CDKN2B, MTAP, and NF2 in 2 mesotheliomas and of BAP1 and TP53 in 1 mesothelioma each, respectively. In addition, 1 patient harbored a pathogenic BRCA1 germline mutation, which resulted in biallelic inactivation in the mesothelioma. All mesotheliomas were mismatch repair proficient and showed several chromosomal gains and losses. All patients died from disease. Our study demonstrates that pericardial mesotheliomas share common morphologic, immunohistochemical, and molecular genetic features with pleural mesothelioma, including recurrent genomic inactivation of canonical tumor suppressors. Our study adds new insights into the genetic landscape of primary pericardial mesothelioma and highlights BRCA1 loss as a potential contributing factor in a subset of cases, thereby contributing to refined precision diagnostics for this rare cancer.

Indexed as

Heart NeoplasmsLung NeoplasmsMesotheliomaMesothelioma, MalignantPleural NeoplasmsThymus NeoplasmsAgedBiomarkers, TumorFemaleHumansMaleNeoplasm Recurrence, LocalUbiquitin ThiolesteraseBiomarkers, TumorUbiquitin ThiolesteraseasbestosBRCA1cell cycle regulatorgermlinemesotheliomanext-generation sequencingpericardiumtumor suppressor

Identifiers

PMID37295554
PMCPMC10529127
OpenAlexW4379883498

What OpenQuestion holds

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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.