Evidence map›Paper›PMID 20708618›Full record

ArticleGastroenterology2010

Microsatellite alterations at selected tetranucleotide repeats are associated with morphologies of colorectal neoplasias.

Sun-Young Lee, Heekyung Chung, Bikash Devaraj, Moriya Iwaizumi, Hye Seung Han, Dae-Yong Hwang, Moo Kyung Seong, Barbara H Jung, John M Carethers

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

55 citing papers in PubMed, 77 citations in OpenAlex.

  1. Trial
  2. THE JEREMIAH METZGER LECTURE: ENVIRONMENTAL INFLUENCES ON COLORECTAL CANCER.Transactions of the American Clinical and Climatological Association · 2024
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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 2 countries.

Sun-Young LeeDepartment of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea.
Heekyung Chung
Bikash Devaraj
Moriya Iwaizumi
Hye Seung Han
Dae-Yong Hwang
Moo Kyung Seong
Barbara H Jung
John M Carethers
University of California, San Diego · USKonkuk University · KRUniversity of Michigan–Ann Arbor · US

Funding

Research Education CoreU54CA132384 · NCI · SAN DIEGO STATE UNIVERSITY · PI CRIPPS, RICHARD MATTHEW, CROWE, SHEILA E. · 2008 to 2022
$20.7M
Research Education CoreU54CA132379 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ARREDONDO, ELVA M, CROWE, SHEILA E. · 2008 to 2021
$16.1M
MICROSATELLITE INSTABILITY &DNA MISMATCH REPAIR SYSTEMR01DK067287 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CARETHERS, JOHN M · 2005 to 2015
$3.2M
The UCSD Digestive Diseases Research Development CenterR24DK080506 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ECKMANN, LARS · 2008 to 2012
$2.7M
NCI NIH HHS CA132379NCI NIH HHS CA132384NCI NIH HHS U54 CA132379NCI NIH HHS U54 CA132384NIDDK NIH HHS DK067287NIDDK NIH HHS DK080506NIDDK NIH HHS R01 DK067287NIDDK NIH HHS R24 DK080506
6 · The paper itself

Abstract

BACKGROUND &

aimsElevated microsatellite alterations at selected tetranucleotide repeats (EMAST) occurs during microsatellite instability (MSI) that is not associated with major defects in DNA mismatch repair (MMR) but rather the reduced (heterogenous) expression of the MMR protein hMSH3; it occurs in sporadic colorectal tumors. We examined the timing of development of EMAST during progression of colorectal neoplasias and looked for correlations between EMAST and clinical and pathology features of tumors.

methodsWe evaluated tumor samples from a cohort of patients that had 24 adenomas and 84 colorectal cancers. EMAST were analyzed after DNA microdissection of matched normal and tumor samples using the polymorphic tetranucleotide microsatellite markers MYCL1, D9S242, D20S85, D8S321, and D20S82; data were compared with clinical and pathology findings. Traditional MSI analysis was performed and hMSH3 expression was measured.

resultsModerately differentiated adenocarcinomas and poorly differentiated adenocarcinomas had higher frequencies of EMAST (56.9% and 40.0%, respectively) than well-differentiated adenocarcinomas (12.5%) or adenomas (33.3%) (P = .040). In endoscopic analysis, ulcerated tumors had a higher frequency of EMAST (52.3%) than flat (44.0%) or protruded tumors (20.0%) (P = .049). In quantification, all tumors with >3 tetranucleotide defects lost MSH3 (>75% of cells); nuclear heterogeneity of hMSH3 occurred more frequently in EMAST-positive (40.0%) than in EMAST-negative tumors (13.2%) (P = .010).

conclusionsEMAST is acquired during progression of adenoma and well-differentiated carcinomas to moderately and poorly differentiated carcinomas; it correlates with nuclear heterogeneity for hMSH3. Loss of hMSH3 corresponds with multiple tetranucleotide frameshifts. The association between EMAST and ulcerated tumors might result from increased inflammation.

Indexed as

Gene Expression Regulation, NeoplasticBase Pair MismatchColonoscopyColorectal NeoplasmsDNA-Binding ProteinsDNA, NeoplasmFemaleHumansImmunohistochemistryMaleMicrosatellite RepeatsMiddle AgedMutS Homolog 3 ProteinPolymerase Chain ReactionDNA-Binding ProteinsDNA, NeoplasmMSH3 protein, humanMutS Homolog 3 Protein

Identifiers

PMID20708618
PMCPMC2967646
OpenAlexW2026819054

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.