Evidence map›Paper›PMID 23593308›Full record

ArticlePloS one2013

The leptin gene family and colorectal cancer: interaction with smoking behavior and family history of cancer.

Li Liu, Rong Zhong, Sheng Wei, Hao Xiang, Jigui Chen, Duoshuang Xie, Jieyun Yin, Li Zou, Jingwen Sun, Wei Chen and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
1.6field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. LEP gene variant is associated with prostate cancer but not with colorectal cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Pooled it
  3. Trial
  4. Article
  5. Article
  6. Leptin Signaling in Obesity and Colorectal Cancer.International journal of molecular sciences · 2022
    Review
  7. Article
  8. XRCC2 Polymorphisms and Environmental Factors Predict High Risk of Colorectal Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Genetic Variations inIranian journal of cancer prevention · 2016
    Article
  14. Article
  15. Article
  16. Role of dysregulated expression of leptin and leptin receptors in colorectal carcinogenesis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Review
  17. Review
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

12 authors at 4 institutions in 1 country.

Li LiuDepartment of Epidemiology and Biostatistics, and the Ministry of Education Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Rong Zhong
Sheng Wei
Hao Xiang
Jigui Chen
Duoshuang Xie
Jieyun Yin
Li Zou
Jingwen Sun
Wei Chen
Xiaoping Miao
Shaofa Nie
Huazhong University of Science and Technology · CNTaihe Hospital · CNThe Eighth Hospital of Xi'an · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPathologic condition associated with metabolic syndrome traits seems to increase the risk of colorectal cancer. One mechanism underlying this relationship may involve the growth-promoting effects of the circulation hormones associated with obesity and insulin resistance, such as leptin. METHODOLOGY/PRINCIPAL

findingsA two-stage case-control study was used to explore the role of polymorphisms of Leptin (LEP) and Leptin receptor (LEPR), either alone or in combination with environmental factors in colorectal carcinogenesis. In stage 1, 20 single nucleotide polymorphisms (SNPs) that tag common SNPs in these two genes were genotyped among 470 cases and 458 controls. In stage 2, another population with 314 cases and 355 controls were genotyped for the two most promising SNPs from stage 1. LEPR rs12037879 only presented modestly increased colorectal cancer risk, with odds ratios of 1.41 (95% confidence interval [CI] 1.13-1.76) and 1.74 (95%CI 1.08-2.81) for GA and AA genotype when compared with GG genotype in combined population. Smokers carrying LEPR rs12037879 A allele presented 1.67-fold (95%CI 1.39-fold to 2.01-fold) increased colorectal cancer risk when compared with non-smokers carrying GG genotype in combined analysis. Individuals with family history of cancer harboring LEPR rs12037879 A allele showed 1.52-fold (95%CI: 1.24-fold to 1.86-fold) increased colorectal cancer risk, compared with individuals without family history of cancer harboring GG genotype. Multifactor gene-environment interaction analysis revealed significant interactions among LEPR rs12037879, LEPR rs6690625, smoking status and family history of cancer, exhibiting a gradient of increased colorectal cancer risk along with the increasing number of risk factors (P = 9.82 × 10(-10)). CONCLUSIONS/SIGNIFICANCE: Our research supports that polymorphisms in LEPR may be associated with marginal increase in the risk for colorectal cancer. Moreover, this association could be strengthened by cigarette smoking and family history of cancer.

Indexed as

Gene-Environment InteractionPedigreePolymorphism, Single NucleotideCase-Control StudiesColorectal NeoplasmsFemaleGenetic Predisposition to DiseaseHumansLeptinMaleMiddle AgedReceptors, LeptinSmokingLeptinReceptors, Leptin

Identifiers

PMID23593308
PMCPMC3620466
OpenAlexW2077296319

What OpenQuestion holds

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LicenceCC BY
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.