Evidence map›Paper›PMID 25214859›Full record

ArticleKorean journal of pathology2014

Differential Features of Microsatellite-Unstable Colorectal Carcinomas Depending on EPCAM Expression Status.

Jung Ho Kim, Jeong Mo Bae, Kyung-Ju Kim, Ye-Young Rhee, Younghoon Kim, Nam-Yun Cho, Hye Seung Lee, Mee Soo Chang, Gyeong Hoon Kang

Open access · diamondAbstract read
In one paragraph

Article in Korean journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

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  12. Clinical and prognostic value of MET gene copy number gain and chromosome 7 polysomy in primary colorectal cancer patients.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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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 3 institutions in 1 country.

Jung Ho KimDepartment of Pathology, SMG-SNU Boramae Medical Center, Seoul, Korea.
Jeong Mo BaeDepartment of Pathology, Seoul National University College of Medicine, Seoul, Korea.
Kyung-Ju KimDepartment of Pathology, Seoul National University College of Medicine, Seoul, Korea.
Ye-Young RheeDepartment of Pathology, Seoul National University College of Medicine, Seoul, Korea.
Younghoon KimDepartment of Pathology, Seoul National University College of Medicine, Seoul, Korea.
Nam-Yun ChoLaboratory of Epigenetics, Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Hye Seung LeeDepartment of Pathology, Seoul National University Bundang Hospital, Seongnam, Korea.
Mee Soo ChangDepartment of Pathology, SMG-SNU Boramae Medical Center, Seoul, Korea. ; Department of Pathology, Seoul National University College of Medicine, Seoul, Korea.
Gyeong Hoon KangDepartment of Pathology, Seoul National University College of Medicine, Seoul, Korea. ; Laboratory of Epigenetics, Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Seoul National University · KRSeoul National University Bundang Hospital · KRSNUH SMG-SNU Boramae Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent studies have revealed that a small subset of Lynch syndrome-associated colorectal carcinomas (CRCs) is caused by a germline EPCAM deletion-induced MSH2 epimutation. Based on the finding of this genetic alteration, we investigated the implications of EPCAM expression changes in microsatellite instability-high (MSI-H) CRCs.

methodsExpression of EPCAM and DNA mismatch repair proteins was assessed by immunohistochemistry in 168 MSI-H CRCs. Using DNA samples of these tumors, MLH1 promoter methylation status was also determined by methylation-specific real-time polymerase chain reaction method (MethyLight).

resultsAmong 168 MSI-H CRCs, complete loss (CL) and focal loss (FL) of EPCAM expression was observed in two (1.2%) and 22 (13.1%) cases, respectively. Both of the EPCAM-CL cases were found in MSH2-negative tumors without MLH1 promoter methylation. However, only nine of the 22 EPCAM-FL tumors had MSH2 deficiency. Of the 22 EPCAM-FL tumors, 13 showed MLH1 loss, and among them, nine cases were determined to have MLH1 methylation. EPCAM-FL was significantly associated with advanced stage (p=.043), distant metastasis (p=.003), poor differentiation (p=.001), and signet ring cell component (p=.004).

conclusionsLoss of EPCAM expression is differentially associated with clinicopathological and molecular features, depending on the completeness of the loss, in MSI-H CRCs.

Indexed as

Colorectal neoplasmsDNA mismatch repairEPCAMMicrosatellite instability

Identifiers

PMID25214859
PMCPMC4160590
OpenAlexW2104962559

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

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.