Evidence map›Paper›PMID 27148484›Full record

ArticleFrontiers in oncology2016

Differences of Variable Number Tandem Repeats in XRCC5 Promoter Are Associated with Increased or Decreased Risk of Breast Cancer in BRCA Gene Mutation Carriers.

Jian Cui, Jiangtao Luo, Yeong C Kim, Carrie Snyder, Dina Becirovic, Bradley Downs, Henry Lynch, San Ming Wang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

3 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Genetic association ofOncoTargets and therapy · 2019
    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

8 authors at 2 institutions in 1 country.

Jian CuiDepartment of Genetics, Cell Biology and Anatomy, College of Medicine, University of Nebraska Medical Center , Omaha, NE , USA.
Jiangtao LuoDepartment of Biostatistics, College of Public Health, University of Nebraska Medical Center , Omaha, NE , USA.
Yeong C KimDepartment of Genetics, Cell Biology and Anatomy, College of Medicine, University of Nebraska Medical Center , Omaha, NE , USA.
Carrie SnyderDepartment of Preventive Medicine, Hereditary Cancer Center, Creighton University , Omaha, NE , USA.
Dina BecirovicDepartment of Preventive Medicine, Hereditary Cancer Center, Creighton University , Omaha, NE , USA.
Bradley DownsDepartment of Genetics, Cell Biology and Anatomy, College of Medicine, University of Nebraska Medical Center , Omaha, NE , USA.
Henry LynchDepartment of Preventive Medicine, Hereditary Cancer Center, Creighton University , Omaha, NE , USA.
San Ming WangDepartment of Genetics, Cell Biology and Anatomy, College of Medicine, University of Nebraska Medical Center , Omaha, NE , USA.
University of Nebraska Medical Center · USCreighton University · US

Funding

(PQD3) Genetic Basis of Breast Cancer Resistance in BRCA1+ CarrierR21CA180008 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WANG, SAN MING · 2013 to 2014
$364k
NCI NIH HHS R21 CA180008
6 · The paper itself

Abstract

Ku80 is a subunit of the Ku heterodimer that binds to DNA double-strand break ends as part of the non-homologous end joining (NHEJ) pathway. Ku80 is also involved in homologous recombination (HR) via its interaction with BRCA1. Ku80 is encoded by the XRCC5 gene that contains a variable number tandem repeat (VNTR) insertion in its promoter region. Different VNTR genotypes can alter XRCC5 expression and affect Ku80 production, thereby affecting NHEJ and HR pathways. VNTR polymorphism is associated with multiple types of sporadic cancer. In this study, we investigated its potential association with familial breast cancer at the germline level. Using PCR, PAGE, Sanger sequencing, and statistical analyses, we compared VNTR genotypes in the XRCC5 promoter between healthy individuals and three types of familial breast cancer cases: mutated BRCA1 (BRCA1 (+)), mutated BRCA2 (BRCA2 (+)), and wild-type BRCA1/BRCA2 (BRCAx). We observed significant differences of VNTR genotypes between control and BRCA1 (+) group (P < 0.0001) and BRCA2 (+) group (P = 0.0042) but not BRCAx group (P = 0.2185), and the differences were significant between control and cancer-affected BRCA1 (+) cases (P < 0.0001) and BRCA2 (+) cases (P = 0.0092) but not cancer-affected BRCAx cases (P = 0.4251). Further analysis indicated that 2R/2R (OR = 1.94, 95%CI = 1.26-2.95, P = 0.0096) and 2R/1R (OR = 1.58, 95%CI = 1.11-2.26, P = 0.0388) were associated with increased risk but 1R/1R (OR = 0.55, 95%CI = 0.35-0.84, P = 0.0196) and 1R/0R (OR = 0, 95%CI = 0-0.29, P = 0.0012) were associated with decreased risk in cancer-affected BRCA1 (+) group; 2R/1R (OR = 1.94, 95%CI = 1.14-3.32, P = 0.0242) was associated with increased risk in cancer-affected BRCA2 (+) group. No correlation was observed for the altered risk between cancer-affected or -unaffected carriers and between different age of cancer diagnosis in cancer-affected carriers. The frequently observed VNTR association with in BRCA1 (+) and BRCA2 (+) breast cancer group indicates that VNTR polymorphism in the XRCC5 promoter is associated with altered risk of breast cancer in BRCA1 (+) and BRCA2 (+) carriers.

Indexed as

associationBRCA1BRCA2familial breast cancerKu80promoterVNTRXRCC5

Identifiers

PMID27148484
PMCPMC4829605
OpenAlexW2342384326

What OpenQuestion holds

Textmetadata
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.