Evidence map›Paper›PMID 26362652›Full record

Trial reportJournal of biomedical science2015

Gene-gene interaction analysis identifies a new genetic risk factor for colorectal cancer.

Jongkeun Park, Injung Kim, Keum Ji Jung, Soriul Kim, Sun Ha Jee, Sungjoo Kim Yoon

Open access · diamondAbstract readClinical TrialMulticenter Study
In one paragraph

Trial report in Journal of biomedical science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Association of CDH13 Gene Polymorphism and Metabolic Syndrome in Gambian Population.Medical archives (Sarajevo, Bosnia and Herzegovina) · 2021
    Article
  5. Article
  6. Article
  7. Article
  8. Genetic variation inOncotarget · 2018
    Article
  9. Article
  10. Article
  11. Genetic variationOncoTargets and therapy · 2016
    Article
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

6 authors at 3 institutions in 1 country.

Jongkeun ParkDepartment of Medical Lifesciences, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, Seoul, 137-701, Republic of Korea.
Injung KimDepartment of Medical Lifesciences, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, Seoul, 137-701, Republic of Korea.
Keum Ji JungDepartment of Epidemiology and Health Promotion, Institute for Health Promotion, Graduate School of Public Health, Yonsei University, Seoul, South Korea.
Soriul KimDepartment of Epidemiology and Health Promotion, Institute for Health Promotion, Graduate School of Public Health, Yonsei University, Seoul, South Korea.
Sun Ha JeeDepartment of Epidemiology and Health Promotion, Institute for Health Promotion, Graduate School of Public Health, Yonsei University, Seoul, South Korea.
Sungjoo Kim YoonDepartment of Medical Lifesciences, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, Seoul, 137-701, Republic of Korea. sjkyoon@catholic.ac.kr.
Catholic University of Korea · KRKorea Health Promotion Institute · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAdiponectin levels have been shown to be associated with colorectal cancer (CRC). Furthermore, a newly identified adiponectin receptor, T-cadherin, has been associated with plasma adiponectin levels. Therefore, we investigated the potential for a genetic association between T-cadherin and CRC risk.

resultWe conducted a case-control study using the Korean Cancer Prevention study-II cohort, which is composed of 325 CRC patients and 977 normal individuals. Study results revealed that rs3865188 in the 5' flanking region of the T-cadherin gene (CDH13) was significantly associated with CRC (p = 0.0474). The odds ratio (OR) for the TT genotype as compared to the TA + AA genotype was 1.577 (p = 0.0144). In addition, the interaction between CDH13 and the adiponectin gene (APN) for CRC risk was investigated using a logistic regression analysis. Among six APN single nucleotide polymorphisms (rs182052, rs17366568, rs2241767, rs3821799, rs3774261, and rs6773957), an interaction with the rs3865188 was found for four (rs2241767, rs3821799, rs3774261, and rs6773957). The group with combined genotypes of TT for rs3865188 and GG for rs377426 displayed the highest risk for CRC development as compared to those with the other genotype combinations. The OR for the TT/GG genotype as compared to the AA/AA genotype was 4.108 (p = 0.004). Furthermore, the plasma adiponectin level showed a correlation with the gene-gene interaction, and the group with the highest risk for CRC had the lowest adiponectin level (median, 4.8 μg/mL for the TT/GG genotype vs.7.835 μg/mL for the AA/AA genotype, p = 0.0017).

conclusionsThe present study identified a new genetic factor for CRC risk and an interaction between CDH13 and APN in CRC risk. These genetic factors may be useful for predicting CRC risk.

Indexed as

Epistasis, GeneticPolymorphism, Single NucleotideAdiponectinAdultCadherinsColorectal NeoplasmsFemaleGenotypeHumansMaleMiddle AgedNeoplasm ProteinsRisk FactorsAdiponectinADIPOQ protein, humanCadherinsH-cadherinNeoplasm Proteins

Identifiers

PMID26362652
PMCPMC4566297
OpenAlexW2103723120

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.