Evidence map›Paper›PMID 19846565›Full record

ArticleAmerican journal of epidemiology2009

Genetic variation in the progesterone receptor and metabolism pathways and hormone therapy in relation to breast cancer risk.

Kerryn W Reding, Christopher I Li, Noel S Weiss, Chu Chen, Christopher S Carlson, David Duggan, Kenneth E Thummel, Janet R Daling, Kathleen E Malone

Open access · bronzeAbstract read
In one paragraph

Article in American journal of epidemiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 5 pooled it
0.8field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 5 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. Pooled it
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  4. Association between the CYP3A4 and CYP3A5 polymorphisms and cancer risk: a meta-analysis and meta-regression.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

9 authors at 3 institutions in 1 country.

Kerryn W RedingDepartment of Epidemiology, School of Public Health, University of Washington, Seattle, Washington 98109, USA. kreding@u.washington.edu
Christopher I Li
Noel S Weiss
Chu Chen
Christopher S Carlson
David Duggan
Kenneth E Thummel
Janet R Daling
Kathleen E Malone
Fred Hutch Cancer Center · USUniversity of Washington · USTranslational Genomics Research Institute · US

Funding

Developing Data-Driven Cancer ResearchersT32CA009168 · NCI · UNIVERSITY OF WASHINGTON · PI STEPHEN M SCHWARTZ, MICHAEL Chiao-An WU · 1985 to 2026
$10.1M
Breast cancer prognostic factors/pathobiologyR01CA098858 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI MALONE, KATHLEEN E · 2004 to 2009
$5.2M
HRT USE AND RISK OF LOBULAR AND DUCTAL BREAST CANCERR01CA085913 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI DALING, JANET R · 2000 to 2004
$2.8M
CALCIUM CHANNEL BLOCKERS IN BREAST CANCER ETIOLOGYR01CA072787 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI DALING, JANET R · 1997 to 2001
$704k
Breast cancer and HRT: genetic susceptibility within th*R03CA119746 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI MALONE, KATHLEEN E · 2005 to 2006
$171k
NCI NIH HHS R01 CA085913NCI NIH HHS R01 CA098858NCI NIH HHS R01 CA72787NCI NIH HHS R01 CA85913NCI NIH HHS R03 CA119746NCI NIH HHS T32 CA009168NCI NIH HHS T32 CA09168
6 · The paper itself

Abstract

The relevance of progesterone to breast carcinogenesis is highlighted by evidence indicating that use of combined estrogen-progesterone therapy (EPT) is more strongly related to breast cancer risk than is use of unopposed estrogen therapy. However, few investigators have assessed how genetic variation in progesterone-related genes modifies the effect of EPT on risk. In an analysis combining data from 2 population-based case-control studies of postmenopausal breast cancer (1,296 cases and 1,055 controls) conducted in Washington State in 1997-1999 and 2000-2004, the authors evaluated how 51 single nucleotide polymorphisms in 7 progesterone-related genes (AKR1C1, AKR1C2, AKR1C3, CYP3A4, SRD5A1, SRD5A2, and PGR) influenced breast cancer risk. There was no appreciable association with breast cancer risk overall for any single nucleotide polymorphism. For rs2854482 in AKR1C2, carrying 1 or 2 A alleles was associated with a 2.0-fold increased breast cancer risk in EPT users (95% confidence interval: 1.0, 4.0) but not in never users (P(heterogeneity) = 0.03). For rs12387 in AKR1C3, the presence of 1 or 2 G alleles was associated with a 1.5-fold increased risk among EPT users (95% confidence interval: 1.1, 2.2) but not in never users (P(heterogeneity) = 0.02). Interpretation of these subgroup associations must await the results of similar studies conducted in other populations.

Indexed as

Polymorphism, Single Nucleotide3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)3-Hydroxysteroid DehydrogenasesAgedAldo-Keto Reductase Family 1 Member C3Breast NeoplasmsCase-Control StudiesConfidence IntervalsEstrogen Replacement TherapyFemaleGenetic VariationHumansHydroxyprostaglandin DehydrogenasesHydroxysteroid DehydrogenasesOdds RatioPostmenopause3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)3-Hydroxysteroid DehydrogenasesAKR1C2 protein, humanAKR1C3 protein, humanAldo-Keto Reductase Family 1 Member C3Hydroxyprostaglandin DehydrogenasesHydroxysteroid DehydrogenasesReceptors, EstrogenReceptors, Progesterone

Identifiers

PMID19846565
PMCPMC2781763
OpenAlexW2145622338

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.