Evidence map›Paper›PMID 21642358›Full record

ArticleCarcinogenesis2011

Common genetic variants related to genomic integrity and risk of papillary thyroid cancer.

Gila Neta, Alina V Brenner, Erich M Sturgis, Ruth M Pfeiffer, Amy A Hutchinson, Briseis Aschebrook-Kilfoy, Meredith Yeager, Li Xu, William Wheeler, Michael Abend and 4 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Carcinogenesis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Epigenetic heterogeneity in cancer.Biomarker research · 2019
    Review
  11. Germline Variants in DNA Repair Genes, Diagnostic Radiation, and Risk of Thyroid Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

14 authors at 5 institutions in 1 country.

Gila NetaRadiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health/DHHS, 6120 Executive Boulevard, Rockville, MD 20852-7244, USA. netagil@mail.nih.gov
Alina V Brenner
Erich M Sturgis
Ruth M Pfeiffer
Amy A Hutchinson
Briseis Aschebrook-Kilfoy
Meredith Yeager
Li Xu
William Wheeler
Michael Abend
Elaine Ron
Margaret A Tucker
Stephen J Chanock
Alice J Sigurdson
National Institutes of Health · USScience Applications International Corporation (United States) · USInformation Management Services · USInstitut für Radiobiologie der BundeswehrThe University of Texas MD Anderson Cancer Center · US

Funding

Studies of Populations Exposed to Occupational Sources of RadiationZIACP010133 · NCI · DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS · PI KITAHARA, CARI · 2009 to 2025
$34.2M
Intramural NIH HHS
6 · The paper itself

Abstract

DNA damage is an important mechanism in carcinogenesis, so genes related to maintaining genomic integrity may influence papillary thyroid cancer (PTC) risk. Candidate gene studies targeting some of these genes have identified only a few polymorphisms associated with risk of PTC. Here, we expanded the scope of previous candidate studies by increasing the number and coverage of genes related to maintenance of genomic integrity. We evaluated 5077 tag single-nucleotide polymorphisms (SNPs) from 340 candidate gene regions hypothesized to be involved in DNA repair, epigenetics, tumor suppression, apoptosis, telomere function and cell cycle control and signaling pathways in a case-control study of 344 PTC cases and 452 matched controls. We estimated odds ratios for associations of single SNPs with PTC risk and combined P values for SNPs in the same gene region or pathway to obtain gene region-specific or pathway-specific P values using adaptive rank-truncated product methods. Nine SNPs had P values <0.0005, three of which were in HDAC4 and were inversely related to PTC risk. After multiple comparisons adjustment, no SNPs remained associated with PTC risk. Seven gene regions were associated with PTC risk at P < 0.01, including HUS1, ALKBH3, HDAC4, BAK1, FAF1_CDKN2C, DACT3 and FZD6. Our results suggest a possible role of genes involved in maintenance of genomic integrity in relation to risk of PTC.

Indexed as

Genomic InstabilityAdultAgedAged, 80 and overBiomarkers, TumorCarcinomaCarcinoma, PapillaryCase-Control StudiesFemaleGene Expression ProfilingGenetic Predisposition to DiseaseGenotypeHumansMaleMiddle AgedOligonucleotide Array Sequence AnalysisBiomarkers, Tumor

Identifiers

PMID21642358
PMCPMC3166197
OpenAlexW2124971829

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.