Evidence map›Paper›PMID 18194538›Full record

SynthesisBMC cancer2008

Combined effect of CCND1 and COMT polymorphisms and increased breast cancer risk.

Ummiye V Onay, Kirsimari Aaltonen, Laurent Briollais, Julia A Knight, Noel Pabalan, Outi Kilpivaara, Irene L Andrulis, Carl Blomqvist, Heli Nevanlinna, Hilmi Ozcelik

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in BMC cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 6 pooled it
2.9field-weighted citation impact, top 9% 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, 6 syntheses or guidelines pooled it, 35 citations in OpenAlex.

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  3. Genetic association between cyclin D1 polymorphism and breast cancer susceptibility.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
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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

10 authors at 4 institutions in 2 countries.

Ummiye V OnayFred A, Litwin Centre for Cancer Genetics, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada. venus.onay@sympatico.ca
Kirsimari Aaltonen
Laurent Briollais
Julia A Knight
Noel Pabalan
Outi Kilpivaara
Irene L Andrulis
Carl Blomqvist
Heli Nevanlinna
Hilmi Ozcelik
Helsinki University Hospital · FIMount Sinai Hospital · CALunenfeld-Tanenbaum Research Institute · CAUniversity of Toronto · CA

Funding

Redox Regulation of Metastasis by Sod2K22CA095011 · NCI · ALBANY MEDICAL COLLEGE · PI MELENDEZ, JUAN ANDRES · 2002 to 2004
$446k
NCI NIH HHS CA-95-011
6 · The paper itself

Abstract

backgroundEstrogens are crucial tumorigenic hormones, which impact the cell growth and proliferation during breast cancer development. Estrogens are metabolized by a series of enzymes including COMT, which converts catechol estrogens into biologically non-hazardous methoxyestrogens. Several studies have also shown the relationship between estrogen and cell cycle progression through activation of CCND1 transcription.

methodsIn this study, we have investigated the independent and the combined effects of commonly occurring CCND1 (Pro241Pro, A870G) and COMT (Met108/158Val) polymorphisms to breast cancer risk in two independent Caucasian populations from Ontario (1228 breast cancer cases and 719 population controls) and Finland (728 breast cancer cases and 687 population controls). Both COMT and CCND1 polymorphisms have been previously shown to impact on the enzymatic activity of the coded proteins.

resultsHere, we have shown that the high enzymatic activity genotype of CCND1High (AA) was associated with increased breast cancer risk in both the Ontario [OR: 1.3, 95%CI (1.0-1.69)] and the Finland sample [OR: 1.4, 95%CI (1.01-1.84)]. The heterozygous COMTMedium (MetVal) and the high enzymatic activity of COMTHigh (ValVal) genotype was also associated with breast cancer risk in Ontario cases, [OR: 1.3, 95%CI (1.07-1.68)] and [OR: 1.4, 95%CI (1.07-1.81)], respectively. However, there was neither a statistically significant association nor increased trend of breast cancer risk with COMTHigh (ValVal) genotypes in the Finland cases [OR: 1.0, 95%CI (0.73-1.39)]. In the combined analysis, the higher activity alleles of the COMT and CCND1 is associated with increased breast cancer risk in both Ontario [OR: 2.22, 95%CI (1.49-3.28)] and Finland [OR: 1.73, 95%CI (1.08-2.78)] populations studied. The trend test was statistically significant in both the Ontario and Finland populations across the genotypes associated with increasing enzymatic activity.

conclusionUsing two independent Caucasian populations, we have shown a stronger combined effect of the two commonly occurring CCND1 and COMT genotypes in the context of breast cancer predisposition.

Indexed as

AdultAgedAllelesBreast NeoplasmsCase-Control StudiesCatechol O-MethyltransferaseCyclin DCyclinsFemaleGenetic Predisposition to DiseaseGenotypeHumansMiddle AgedPolymorphism, Single NucleotideCatechol O-MethyltransferaseCyclin DCyclins

Identifiers

PMID18194538
PMCPMC2254632
OpenAlexW2061989615

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.