Evidence map›Paper›PMID 17380277›Full record

ArticleJournal of gastroenterology2007

High polymorphism in the trisomic portion of a gastric cancer cell line.

Blake A Jacobson, James M Fink, Bryan A Whitson, Lance J Ferrin

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Article in Journal of gastroenterology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

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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

1 citing paper in PubMed.

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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

4 authors.

Blake A JacobsonDepartment of Medicine, University of Minnesota, Minneapolis, MN 55455, USA.
James M Fink
Bryan A Whitson
Lance J Ferrin

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenetic instability is a hallmark of malignancy, and microsatellite instability is a widely appreciated mechanism of generating genetic changes. We have recently observed four markers clustered on chromosome 20 that showed the effects of microsatellite instability in the gastric adenocarcinoma cell line SNU-1. Each affected marker had alleles of three different sizes. The aim of this study was to investigate the origin for this high-density polymorphism on a single chromosome.

methodsThe high polymorphism located on chromosome 20 was confirmed using 37 additional markers. To further evaluate this finding, 15 clones of the cell line were generated and then assayed with the triallelic markers.

resultsAll told, almost a third of the markers on chromosome 20 had triallelic patterns, but only 0.3% of the markers not on chromosome 20 showed this result. The number of clones showing allelic variation was an average of 50% greater for chromosome 20 markers than for markers elsewhere. A karyotype analysis showed that the progenitor cell line of SNU-1 was trisomic for chromosome 20, and the high polymorphism on that chromosome is almost certainly due to the trisomy.

conclusionsNot only are there more chromosome copies and therefore more gene copies subject to mutation in cells containing trisomy, but also more mutations may be passed on to the progeny. This elevated polymorphism increases the repertoire of genetic changes that could affect cellular growth, and may independently increase genomic instability.

Indexed as

Polymorphism, GeneticAdenocarcinomaBiomarkers, TumorCell Line, TumorChromosomes, Human, Pair 20HumansKaryotypingMicrosatellite InstabilityPolymerase Chain ReactionStomach NeoplasmsTrisomyBiomarkers, Tumor

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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.