Evidence map›Paper›PMID 21750172›Full record

ArticleCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology2011

Functional polymorphisms in UDP-glucuronosyl transferases and recurrence in tamoxifen-treated breast cancer survivors.

Thomas P Ahern, Mariann Christensen, Deirdre P Cronin-Fenton, Kathryn L Lunetta, Håvard Søiland, Jennifer Gjerde, Jens Peter Garne, Carol L Rosenberg, Rebecca A Silliman, Henrik Toft Sørensen and 2 more

Open access · bronzeAbstract readClinical Trial, Phase I
In one paragraph

Article in Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.1field-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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  6. Review
  7. Genetic Influences in Breast Cancer Drug Resistance.Breast cancer (Dove Medical Press) · 2021
    Review
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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

12 authors at 5 institutions in 3 countries.

Thomas P AhernChanning Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA. nhtpa@channing.harvard.edu
Mariann Christensen
Deirdre P Cronin-Fenton
Kathryn L Lunetta
Håvard Søiland
Jennifer Gjerde
Jens Peter Garne
Carol L Rosenberg
Rebecca A Silliman
Henrik Toft Sørensen
Timothy L Lash
Stephen Hamilton-Dutoit
Aalborg University Hospital · DKAarhus University Hospital · DKBoston University · USHaukeland University Hospital · NOStavanger University Hospital · NO

Funding

Training Program in Cancer EpidemiologyT32CA009001 · NCI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI A. Heather Eliassen, Meir Stampfer · 1985 to 2026
$17.3M
Modification of tamoxifen effectiveness by gene polymorphisms and other drugsR01CA118708 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LASH, TIMOTHY L. · 2006 to 2009
$963k
NCI NIH HHS R01 CA118708NCI NIH HHS T32 CA009001NCI NIH HHS T32 CA09001-35
6 · The paper itself

Abstract

backgroundTamoxifen is oxidized by cytochrome-P450 enzymes (e.g., CYP2D6) to two active metabolites, which are eliminated via glucuronidation by UDP-glucuronosyl transferases (UGT). We measured the association between functional polymorphisms in key UGTs (UGT2B15*2, UGT2B7*2, and UGT1A8*3) and the recurrence rate among breast cancer survivors.

methodsWe used the Danish Breast Cancer Cooperative Group registry to identify 541 cases of recurrent breast cancer among women with estrogen receptor-positive tumors treated with tamoxifen for at least 1 year (ER(+)/TAM(+)), and 300 cases of recurrent breast cancer among women with estrogen receptor-negative tumors who were not treated with tamoxifen (ER(-)/TAM(-)). We matched one control to each case on ER status, menopausal status, stage, calendar period, and county. UGT polymorphisms were genotyped from archived primary tumors. We estimated the recurrence OR for the UGT polymorphisms by using logistic regression models, with and without stratification on CYP2D6*4 genotype.

resultsNo UGT polymorphism was associated with breast cancer recurrence in either the ER(+)/TAM(+) or ER(-)/TAM(-) groups [in the ER(+)/TAM(+) group, compared with two normal alleles: adjusted OR for two UGT2B15*2 variant alleles = 1.0 (95% CI, 0.70-1.5); adjusted OR for two UGT2B7*2 variant alleles = 0.96 (95% CI, 0.65-1.4); adjusted OR for one or two UGT1A8*3 variant alleles = 0.95 (0.49-1.9)]. Associations were similar within strata of CYP2D6*4 genotype.

conclusionsFunctional polymorphisms in key tamoxifen-metabolizing enzymes were not associated with breast cancer recurrence risk. IMPACT: Our results do not support the genotyping of key metabolic enzyme polymorphisms to predict response to tamoxifen therapy.

Indexed as

AdultAgedAntineoplastic Agents, HormonalBreast NeoplasmsFemaleGenotypeGlucuronosyltransferaseHumansMiddle AgedNeoplasm Recurrence, LocalPolymorphism, GeneticTamoxifenAntineoplastic Agents, HormonalGlucuronosyltransferaseTamoxifen

Identifiers

PMID21750172
PMCPMC3169710
OpenAlexW1985380895

What OpenQuestion holds

Textmetadata
LicenceTDM
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.