Evidence map›Paper›PMID 17960397›Full record

ArticleInternational journal of colorectal disease2008

Association of familial colorectal cancer with variants in the E-cadherin (CDH1) and cyclin D1 (CCND1) genes.

Frank Grünhage, Matthias Jungck, Christoph Lamberti, Christine Berg, Ursula Becker, Hildegard Schulte-Witte, Dominik Plassmann, Nils Rahner, Stefan Aretz, Nicolaus Friedrichs and 3 more

Abstract read
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In one paragraph

Article in International journal of colorectal disease, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 10 pooled it
–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

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

25 citing papers in PubMed, 10 syntheses or guidelines pooled it.

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  4. The cyclin D1 (CCND1) G870A polymorphism and lung cancer susceptibility: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
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  16. Investigation ofOncoTargets and therapy · 2016
    Article
  17. The significant association of CCND1 genotypes with colorectal cancer in Taiwan.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  18. TP53 alterations and colorectal cancer predisposition in south Indian population: a case-control study.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
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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

13 authors.

Frank GrünhageDepartment of Internal Medicine I, University Hospital Bonn, University of Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, Germany. frank.gruenhage@ukb.uni-bonn.de
Matthias Jungck
Christoph Lamberti
Christine Berg
Ursula Becker
Hildegard Schulte-Witte
Dominik Plassmann
Nils Rahner
Stefan Aretz
Nicolaus Friedrichs
Reinhard Buettner
Tilman Sauerbruch
Frank Lammert

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAbout 20% of colorectal cancer (CRC) patients show some kind of familiarity, which might be caused by yet unknown combinations of low penetrance susceptibility genes. We aimed to identify genetic factors for familial CRC (fCRC) in a unique study design that includes phenotypic extremes as represented by fCRC cases and 'hyper-normal' controls without CRC history and no adenomatous polyps on colonoscopy. MATERIALS AND

methodsCandidate gene variants were determined by allele-specific amplification (SLC10A2 c.169C>T and c.171G>T) and restriction fragment length polymorphism assays (CCND1 c.870A>G; CDH1 -160C>A; TP53 R72P; VDR T2M). In total, 98 patients with fCRC, 96 patients with sporadic CRC, and 220 hyper-normal controls were included.

resultsThe minor allele of the CDH1 -160C>A polymorphism occurred significantly more often in controls compared to fCRC cases (OR = 0.664; p = 0.042). Homozygosity of the minor allele was significantly associated with affiliation to the control group (OR = 0.577; p = 0.029), indicating that both heterozygous and homozygous carriers of the common allele are at-risk for CRC. With respect to the CCND1 c.870A>G mutation, comparison of fCRC and sporadic CRC cases showed that A/A homozygosity was more common than G/G homozygosity among fCRC patients compared to controls (OR = 2.119; p = 0.045). However, no differences in allele or genotype frequencies were detected between sporadic CRC cases and controls, and no associations were observed for SLC10A2, TP53, and VDR polymorphisms.

conclusionsWe report a potential association of variants in the CCND1 and CDH1 genes with fCRC using a unique study design with phenotypic extremes.

Indexed as

Gene Expression Regulation, NeoplasticPolymorphism, GeneticAdultAgedAntigens, CDCadherinsCase-Control StudiesColonoscopyColorectal NeoplasmsCyclin D1FemaleGene FrequencyGenetic Predisposition to DiseaseHeterozygoteHomozygoteHumansAntigens, CDCadherinsCCND1 protein, humanCDH1 protein, humanCyclin D1

Identifiers

PMID17960397

What OpenQuestion holds

Textmetadata
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.