Evidence map›Paper›PMID 25310854›Full record

ArticleJournal of gynecologic oncology2015

DNA mismatch repair-related protein loss as a prognostic factor in endometrial cancers.

Masafumi Kato, Masashi Takano, Morikazu Miyamoto, Naoki Sasaki, Tomoko Goto, Hitoshi Tsuda, Kenichi Furuya

Open access · diamondAbstract read
In one paragraph

Article in Journal of gynecologic oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Deciphering survival disparities in endometrial cancer: a focus on mismatch repair pathway integrity (systematic review and meta-analysis).Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

7 authors at 1 institution in 1 country.

Masafumi KatoDepartment of Obstetrics and Gynecology, National Defense Medical College Hospital, Tokorozawa, Japan.
Masashi TakanoDepartment of Obstetrics and Gynecology, National Defense Medical College Hospital, Tokorozawa, Japan. mastkn@ndmc.ac.jp.
Morikazu MiyamotoDepartment of Obstetrics and Gynecology, National Defense Medical College Hospital, Tokorozawa, Japan.
Naoki SasakiDepartment of Obstetrics and Gynecology, National Defense Medical College Hospital, Tokorozawa, Japan.
Tomoko GotoDepartment of Obstetrics and Gynecology, National Defense Medical College Hospital, Tokorozawa, Japan.
Hitoshi TsudaDepartment of Basic Pathology, National Defense Medical College Hospital, Tokorozawa, Japan.
Kenichi FuruyaDepartment of Obstetrics and Gynecology, National Defense Medical College Hospital, Tokorozawa, Japan.
National Defense Medical College Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveRecent investigations have revealed DNA mismatch repair (MMR) gene mutations are closely related with carcinogenesis of endometrial cancer; however the impact of MMR protein expression on prognosis is not determined. Correlations between MMR-related protein expression and clinicopathological factors of endometrial cancers are analyzed in the present study.

methodsA total of 191 endometrial cancer tissues treated between 1990 and 2007 in our hospital were enrolled. Immunoreactions for MSH2, MLH1, MSH6, and PMS2 on tissue microarray specimens and clinicopathological features were analyzed retrospectively.

resultsSeventy-six cases (40%) had at least one immunohistochemical alteration in MMR proteins (MMR-deficient group). There were statistically significant differences of histology, International Federation of Gynecology and Obstetrics (FIGO) stage, and histological grade between MMR-deficient group and the other cases (MMR-retained group). Response rate of first-line chemotherapy in evaluable cases was slightly higher in MMR-deficient cases (67% vs. 44%, p=0.34). MMR-deficient cases had significantly better progression-free and overall survival (OS) compared with MMR-retained cases. Multivariate analysis revealed MMR status was an independent prognostic factor for OS in endometrial cancers.

conclusionMMR-related proteins expression was identified as an independent prognostic factor for OS, suggesting that MMR was a key biomarker for further investigations of endometrial cancers.

Indexed as

DNA Mismatch RepairAdaptor Proteins, Signal TransducingAdenosine TriphosphatasesAdultAgedAged, 80 and overBiomarkers, TumorChemotherapy, AdjuvantDNA-Binding ProteinsDNA Repair EnzymesEndometrial NeoplasmsFemaleHumansKaplan-Meier EstimateMiddle AgedMismatch Repair Endonuclease PMS2Adaptor Proteins, Signal TransducingAdenosine TriphosphatasesBiomarkers, TumorDNA-Binding ProteinsDNA Repair EnzymesG-T mismatch-binding proteinMismatch Repair Endonuclease PMS2MLH1 protein, humanMSH2 protein, humanMutL Protein Homolog 1MutS Homolog 2 ProteinNeoplasm ProteinsNuclear ProteinsPMS2 protein, humanBiological MarkersCarcinogenesisDNA Mismatch RepairEndometrial NeoplasmsMultivariate AnalysisRetrospective Studies

Identifiers

PMID25310854
PMCPMC4302284
OpenAlexW2120186602

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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.