Evidence map›Paper›PMID 16128738›Full record

ReviewCancer science2005

Genetic polymorphisms of methylenetetrahydrofolate reductase and colorectal cancer and adenoma.

Suminori Kono, Kun Chen

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer science, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 4 pooled it
6.5field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 4 syntheses or guidelines pooled it, 102 citations in OpenAlex.

  1. Pooled it
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  5. MTHFR genotype and colorectal adenoma recurrence: data from a double-blind placebo-controlled clinical trial.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2008
    Trial
  6. Vitamins B2, B6, and B12 and risk of new colorectal adenomas in a randomized trial of aspirin use and folic acid supplementation.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2008
    Trial
  7. Journal of clinical medicine · 2023
    Article
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  14. Colorectal cancer: a researcher's perspective of the molecular angel's gone eccentric in the Vale of Kashmir.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Review
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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

2 authors at 2 institutions in 2 countries.

Suminori KonoDepartment of Preventive Medicine, Faculty of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Fukuoka 812-8582, Japan. skono@phealth.med.kyushu-u.ac.jp
Kun Chen
Kyushu University · JPZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methylenetetrahydrofolate reductase (MTHFR) is a key enzyme regulating folate metabolism, which affects DNA methylation and synthesis. Two functional, common polymorphisms (C677T and A1298C) are known in the MTHFR gene. MTHFR activity is lowered in individuals with the 677TT genotype and is somewhat reduced in those with the 1298CC genotype. We reviewed the consistency of reported associations of these polymorphisms with colorectal cancer and adenoma with consideration of the effects of nutritional status. A total of 16 studies have addressed the association between MTHFR C677T polymorphism and colorectal cancer in 10 countries. Decreased risk of colorectal cancer associated with the 677TT genotype has fairly consistently been observed, with few exceptions. This decrease was observable in people with either high or low folate status. Alteration in the thymidylate pool associated with MTHFR activity is postulated as an underlying mechanism. Studies on the A1298C polymorphism are limited, and their results are variable. Almost all of seven studies of colorectal adenoma have found no association between C677T polymorphism and adenoma, but the 677TT genotype seems to be related to increased risk when folate status is poor. Reduced availability of methyl groups for DNA methylation might be more relevant to adenoma formation. Although the underlying mechanisms still remain to be clarified, epidemiological findings regarding MTHFR C677T polymorphism provide strong evidence that adequate folate status confers protection from colorectal cancer.

Indexed as

Genetic Predisposition to DiseasePolymorphism, GeneticAdenomaColorectal NeoplasmsEpidemiologic StudiesFolic AcidGenotypeHumansMethylenetetrahydrofolate Reductase (NADPH2)Nutritional StatusFolic AcidMethylenetetrahydrofolate Reductase (NADPH2)

Identifiers

PMID16128738
PMCPMC11160001
OpenAlexW2002519571

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.