Evidence map›Paper›PMID 29972732›Full record

ArticleCroatian medical journal2018

Microsatellite instability in metaplasia-dysplasia-adenocarcinoma sequence of Barrett esophagus: a retrospective study.

Pave Markoš, Iva Brčić, Luka Brčić, Jasminka Jakić-Razumović, Roland Pulanić

Abstract read
In one paragraph

Article in Croatian medical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Intervention of RT-ABCDEF for cancer.Croatian medical journal · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Pave MarkošPave Markoš, Division of Gastroenterology and Hepatology, University Hospital Center Zagreb, Kišpatićeva 12, 10000 Zagreb, Croatia, pave.markos@gmail.com.
Iva Brčić
Luka Brčić
Jasminka Jakić-Razumović
Roland Pulanić

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo analyze the loss of mismatch repair (MMR) system protein expression in metaplasia-dysplasia-adenocarcinoma sequence of Barrett esophagus (BE).

methodsThis study retrospectively analyzed the data from 70 patients with pathohistological diagnosis of BE or esophageal adenocarcinoma (EAC) treated at the Clinical Department of Pathology and Cytology, University Hospital Center Zagreb, from January 2009 to January 2011. Patients were divided into three groups: BE without dysplasia (22 patients), BE with dysplasia (37 patients), and EAC (11 patients). Immunohistochemical expression of MutL homologue 1 (MLH1), MutS homologue 2 (MSH2), postmeiotic segregation increased 2 (PMS2), and MutS homologue 6 (MSH6) of DNA MMR system was measured and compared with tumor protein p53 expression.

resultsA total of 81.8% and 81.8% patients with EAC, 32.4% and 35.1% patients with dysplasia, and 50% and 54.5% patients without dysplasia had loss of MLH1 and PMS2 expression, respectively. Patients with EAC and patients with dysplasia did not have loss of MSH2 and MSH6 expression, and 18.2% patients without dysplasia had loss of MSH2 and MSH6 expression. There was a strong positive correlation between MLH1 and PMS2 expression (Spearman ρ 0.97; P<0.001) and between MSH2 and MSH6 expression (Spearman ρ 0.90, P<0.001) in the entire sample and in all BE groups. No significant correlations of MLH1 and PMS2 with p53 expression were found, except in dysplasia group (φ 0.402, P=0.030 for MSH1; φ 0.371, P=0.042 for PMS2).

conclusionAlthough we demonstrated considerable loss of MLH1 and PMS2 expression in BE-associated carcinoma sequence, due to the retrospective study design and low number of patients we cannot conclude that MLH1 and PMS2 can be used as biomarkers for patient surveillance and therapy-making decisions. Oxford Centre for Evidence-based Medicine level of evidence: 3.

Indexed as

Microsatellite InstabilityAdenocarcinomaAdultAgedBarrett EsophagusBiomarkers, TumorDNA-Binding ProteinsDNA Mismatch RepairEsophageal NeoplasmsFemaleHumansImmunoenzyme TechniquesMaleMetaplasiaMiddle AgedMismatch Repair Endonuclease PMS2Biomarkers, TumorDNA-Binding ProteinsG-T mismatch-binding proteinMismatch Repair Endonuclease PMS2MLH1 protein, humanMSH2 protein, humanMutL Protein Homolog 1MutS Homolog 2 ProteinNeoplasm ProteinsPMS2 protein, humanTumor Suppressor Protein p53

Identifiers

PMID29972732
PMCPMC6045894

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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.