Evidence map›Paper›PMID 30883040›Full record

ArticleCancer medicine2019

Association between polymorphisms in MicroRNA target sites of RAD51D genes and risk of hepatocellular carcinoma.

Yan-Ji Jiang, Jian-Hong Zhong, Zi-Han Zhou, Mo-Qin Qiu, Xian-Guo Zhou, Ying-Chun Liu, Rong-Rui Huo, Xiu-Mei Liang, Zhu Chen, Qiu-Ling Lin and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 41% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. BioMed research international · 2020
    Article
  5. MicroRNA heterogeneity in melanoma progression.Seminars in cancer biology · 2019
    Review
  6. 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

12 authors at 3 institutions in 1 country.

Yan-Ji JiangAffiliated Tumor Hospital of Guangxi Medical University, Guangxi, China.ORCID 0000-0003-1751-9645
Jian-Hong ZhongAffiliated Tumor Hospital of Guangxi Medical University, Guangxi, China.ORCID 0000-0002-1494-6396
Zi-Han ZhouAffiliated Tumor Hospital of Guangxi Medical University, Guangxi, China.
Mo-Qin QiuAffiliated Tumor Hospital of Guangxi Medical University, Guangxi, China.
Xian-Guo ZhouAffiliated Tumor Hospital of Guangxi Medical University, Guangxi, China.
Ying-Chun LiuAffiliated Tumor Hospital of Guangxi Medical University, Guangxi, China.
Rong-Rui HuoAffiliated Tumor Hospital of Guangxi Medical University, Guangxi, China.
Xiu-Mei LiangAffiliated Tumor Hospital of Guangxi Medical University, Guangxi, China.
Zhu ChenAffiliated Hospital of Guilin Medical University, Guangxi, China.
Qiu-Ling LinAffiliated Tumor Hospital of Guangxi Medical University, Guangxi, China.
Xiang-Yuan YuSchool of Public Health, Guilin Medical University, Guangxi, China.
Hong-Ping YuAffiliated Tumor Hospital of Guangxi Medical University, Guangxi, China.
Guangxi Medical University · CNTumor Hospital of Guangxi Medical University · CNGuilin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RAD51D (RAD51L3) is a member of the RAD51 gene family which plays important roles in maintaining genomic stability and preventing DNA damage. This study is aimed to investigate the associations between RAD51D polymorphisms and the hereditary susceptibility of hepatocellular carcinoma (HCC). In this study we conducted a hospital-based case-control study including 805 cases (HCC patients) and 846 controls (nontumor patients) in Guangxi, China. A total of two Single-nucleotide polymorphisms (SNPs) rs12947947 and rs28363292 of RAD51D were selected and genotyped. Although we did not find two SNPs individually that had any significant main effect on risk of HCC, We found that the combined genotypes with 1-2 risk genotypes were associated with significantly increased overall risk of HCC (OR = 1.462, 95% CI = 1.050-2.036). According to the results of further stratification analysis, GT/GG genotype of rs28363292 increased HCC risk in zhuang people (OR = 3.913, 95% CI = 1.873-8.175) and nonhepatitis B virus (HBV) infection population (OR = 1.774, 95% CI = 1.060-2.969), the combined 1-2 risk genotypes increased the risk of HCC in zhuang people (OR = 2.817, 95% CI = 1.532-5.182) and non-HBV infected population (OR = 1.567, 95% CI = 1.042-2.358). Our results suggest that rs12947947 and rs28363292 polymorphisms may jointly contribute to the risk of HCC. Further large studies and functional studies are required to validate our findings.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdultAgedAllelesAsian PeopleBinding SitesCarcinoma, HepatocellularCase-Control StudiesDNA-Binding ProteinsFemaleGene FrequencyGenotypeHaplotypesHumansLinkage DisequilibriumDNA-Binding ProteinsMicroRNAsRAD51D protein, humanhepatocellular carcinomaRAD51Dsingle-nucleotide polymorphismsusceptibility

Identifiers

PMID30883040
PMCPMC6536933
OpenAlexW2921294676

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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.