Evidence map›Paper›PMID 27624283›Full record

Trial reportScientific reports2016

MDM2 promoter SNP55 (rs2870820) affects risk of colon cancer but not breast-, lung-, or prostate cancer.

Reham Helwa, Liv B Gansmo, Pål Romundstad, Kristian Hveem, Lars Vatten, Bríd M Ryan, Curtis C Harris, Per E Lønning, Stian Knappskog

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 33% 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, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. 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

9 authors at 4 institutions in 2 countries.

Reham HelwaSection of Oncology, Department of Clinical Science, University of Bergen, 5020 Bergen, Norway.
Liv B GansmoSection of Oncology, Department of Clinical Science, University of Bergen, 5020 Bergen, Norway.
Pål RomundstadDepartment of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, 7489 Trondheim, Norway.
Kristian HveemDepartment of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, 7489 Trondheim, Norway.
Lars VattenDepartment of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, 7489 Trondheim, Norway.
Bríd M RyanLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892, USA.
Curtis C HarrisLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892, USA.
Per E LønningSection of Oncology, Department of Clinical Science, University of Bergen, 5020 Bergen, Norway.
Stian KnappskogSection of Oncology, Department of Clinical Science, University of Bergen, 5020 Bergen, Norway.
Norwegian University of Science and Technology · NOCenter for Cancer Research · USHaukeland University Hospital · NOUniversity of Bergen · NO

Funding

Integrative Molecular Epidemiology of Human CancerZIABC011495 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 2013 to 2019
$9.5M
6 · The paper itself

Abstract

Two functional SNPs (SNP285G > C; rs117039649 and SNP309T > G; rs2279744) have previously been reported to modulate Sp1 transcription factor binding to the promoter of the proto-oncogene MDM2, and to influence cancer risk. Recently, a third SNP (SNP55C > T; rs2870820) was also reported to affect Sp1 binding and MDM2 transcription. In this large population based case-control study, we genotyped MDM2 SNP55 in 10,779 Caucasian individuals, previously genotyped for SNP309 and SNP285, including cases of colon (n = 1,524), lung (n = 1,323), breast (n = 1,709) and prostate cancer (n = 2,488) and 3,735 non-cancer controls, as well as 299 healthy African-Americans. Applying the dominant model, we found an elevated risk of colon cancer among individuals harbouring SNP55TT/CT genotypes compared to the SNP55CC genotype (OR = 1.15; 95% CI = 1.01-1.30). The risk was found to be highest for left-sided colon cancer (OR = 1.21; 95% CI = 1.00-1.45) and among females (OR = 1.32; 95% CI = 1.01-1.74). Assessing combined genotypes, we found the highest risk of colon cancer among individuals harbouring the SNP55TT or CT together with the SNP309TG genotype (OR = 1.21; 95% CI = 1.00-1.46). Supporting the conclusions from the risk estimates, we found colon cancer cases carrying the SNP55TT/CT genotypes to be diagnosed at younger age as compared to SNP55CC (p = 0.053), in particular among patients carrying the SNP309TG/TT genotypes (p = 0.009).

Indexed as

GenotypePolymorphism, Single NucleotidePromoter Regions, GeneticBlack or African AmericanBreast NeoplasmsColonic NeoplasmsFemaleHumansLung NeoplasmsMaleProstatic NeoplasmsProto-Oncogene MasProto-Oncogene Proteins c-mdm2Risk FactorsWhite PeopleMAS1 protein, humanMDM2 protein, humanProto-Oncogene MasProto-Oncogene Proteins c-mdm2

Identifiers

PMID27624283
PMCPMC5022009
OpenAlexW2518993562

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.