Evidence map›Paper›PMID 30532127›Full record

ArticlePloS one2018

Prevalence of elevated microsatellite alterations at selected tetranucleotide repeats in pancreatic ductal adenocarcinoma.

Taiki Mori, Yasushi Hamaya, Takahiro Uotani, Mihoko Yamade, Moriya Iwaizumi, Takahisa Furuta, Hiroaki Miyajima, Satoshi Osawa, Ken Sugimoto

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 2 pooled it
1.3field-weighted citation impact, top 19% 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

8 citing papers in PubMed, 2 syntheses or guidelines pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
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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

9 authors at 1 institution in 1 country.

Taiki MoriFirst Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Yasushi HamayaFirst Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.ORCID 0000-0002-1355-6687
Takahiro UotaniFirst Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Mihoko YamadeFirst Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Moriya IwaizumiLaboratory Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Takahisa FurutaCenter for Clinical Research, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hiroaki MiyajimaFirst Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Satoshi OsawaDepartment of Endoscopic and Photodynamic Medicine, Hamamatsu, Japan.
Ken SugimotoFirst Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hamamatsu University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) prognosis remains poor even after complete resection owing to no valuable biomarkers for recurrence and chemosensitivity. Tumors not expressing MSH3 show elevated microsatellite alterations at selected tetranucleotide repeats (EMAST). EMAST reportedly occurs in several tumors. In colorectal cancer (CRC), EMAST was reportedly correlated with 5-fluorouracil (5-FU) sensitivity. However, EMAST prevalence in PDAC and its significance as a prognostic biomarker are unknown. This study aimed to investigate EMAST prevalence in PDAC and the associations between EMAST and pathological factors, EMAST and prognosis, and EMAST and MSH3 expression via immunohistochemistry (IHC). We assessed 40 PDAC patients undergoing surgery. Genomic DNA was extracted from tumors and normal tissues. EMAST and microsatellite instability-high (MSI-H) were analyzed using five polymorphic tetranucleotide markers and five mononucleotide markers, respectively. Tumor sections were stained for MSH3, and staining intensity was evaluated via the Histoscore (H-score). Eighteen of 40 (45%) PDAC patients were EMAST-positive; however, none were MSI-H-positive. Clinicopathological characteristics including overall survival (OS) and recurrence-free survival (RFS) were not significantly different between EMAST-positive and EMAST-negative patients (P = 0.45, 0.98 respectively). IHC was performed to evaluate MSH3 protein expression levels for the PDAC tissue specimens. H-scores of EMAST-positive patients ranged from 0 to 300 (median, 40) and those of EMAST-negative patients ranged from 0 to 300 (median, 170). MSH3 protein was not significantly downregulated in EMAST-positive patients (P = 0.07). This study is a preliminary study and the number of cases investigated was small, and thus, study of a larger cohort will reveal the clinical implication of EMAST.

Indexed as

AgedAged, 80 and overCarcinoma, Pancreatic DuctalFemaleGene Expression Regulation, NeoplasticHumansMaleMicrosatellite RepeatsMiddle AgedMutS Homolog 3 ProteinPrevalenceMSH3 protein, humanMutS Homolog 3 Protein

Identifiers

PMID30532127
PMCPMC6285458
OpenAlexW2904163034

What OpenQuestion holds

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LicenceCC BY
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.