Evidence map›Paper›PMID 28534527›Full record

ArticleThe pharmacogenomics journal2018

Role of the UGT2B17 deletion in exemestane pharmacogenetics.

S Luo, G Chen, C Truica, C C Baird, K Leitzel, P Lazarus

Open access · hybridAbstract read
In one paragraph

Article in The pharmacogenomics journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 17% 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, 16 citations in OpenAlex.

  1. Review
  2. Impact of combined UGT2B17 and GSTA1 genotypes on exemestane pharmacogenetics.Drug metabolism and disposition: the biological fate of chemicals · 2025
    Article
  3. Article
  4. Article
  5. Molecular pharmacology · 2022
    Article
  6. Review
  7. Characterization of Cytosolic GlutathioneDrug metabolism and disposition: the biological fate of chemicals · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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

6 authors at 2 institutions in 2 countries.

S LuoAlkali Soil Natural Environmental Science Center, Northeast Forestry University, Key Laboratory of Saline-alkali Vegetation Ecology Restoration in Oil Field, Ministry of Education, Harbin, China.
G ChenDepartment of Pharmaceutical Sciences, College of Pharmacy, Washington State University, Spokane, WA, USA.
C TruicaDepartment of Medicine, Penn State University College of Medicine, Hershey, PA, USA.
C C BairdDepartment of Medicine, Penn State University College of Medicine, Hershey, PA, USA.
K LeitzelDepartment of Medicine, Penn State University College of Medicine, Hershey, PA, USA.
P LazarusDepartment of Pharmaceutical Sciences, College of Pharmacy, Washington State University, Spokane, WA, USA.
Penn State Milton S. Hershey Medical Center · USWashington State University Spokane · US

Funding

Role of pharmacogenetics on exemestane metabolism and toxicityR01CA164366 · NCI · WASHINGTON STATE UNIVERSITY · PI LAZARUS, PHILIP · 2012 to 2016
$2.4M
NCI NIH HHS R01 CA164366
6 · The paper itself

Abstract

Exemestane (EXE) is an aromatase inhibitor used for the prevention and treatment of breast cancer. The major metabolic pathway for EXE is reduction to form the active 17β-dihydro-EXE (17β-DHE) and subsequent glucuronidation to 17β-hydroxy-EXE-17-O-β-D-glucuronide (17β-DHE-Gluc) by UGT2B17. The aim of the present study was to determine the effects of UGT2B17 copy number variation on the levels of urinary and plasma 17β-DHE-Gluc and 17β-DHE in patients taking EXE. Ninety-six post-menopausal Caucasian breast cancer patients with ER+ breast tumors taking 25 mg EXE daily were recruited into this study. UGT2B17 copy number was determined by a real-time PCR copy number variant assay and the levels of EXE, 17β-DHE and 17β-DHE-Gluc were quantified by UPLC/MS in patients' urine and plasma. A 39-fold decrease (P<0.0001) in the levels of creatinine-adjusted urinary 17β-DHE-Gluc was observed among UGT2B17 (*2/*2) subjects vs subjects with the UGT2B17 (*1/*1) genotype. The plasma levels of 17β-DHE-Gluc was decreased 29-fold (P<0.0001) in subjects with the UGT2B17 (*2/*2) genotype vs subjects with UGT2B17 (*1/*1) genotype. The levels of plasma EXE-adjusted 17β-DHE was 28% higher (P=0.04) in subjects with the UGT2B17 (*2/*2) genotype vs subjects with the UGT2B17 (*1/*1) genotype. These data indicate that UGT2B17 is the major enzyme responsible for 17β-DHE-Gluc formation in vivo and that the UGT2B17 copy number variant may play a role in inter-individual variability in 17β-DHE levels in vivo.

Indexed as

Gene DeletionAdultAgedAged, 80 and overAndrostadienesAntineoplastic AgentsBreast NeoplasmsFemaleGlucuronosyltransferaseHumansMiddle AgedMinor Histocompatibility AntigensPharmacogeneticsAndrostadienesAntineoplastic AgentsexemestaneGlucuronosyltransferaseMinor Histocompatibility AntigensUGT2B17 protein, human

Identifiers

PMID28534527
PMCPMC5700874
OpenAlexW2618034562

What OpenQuestion holds

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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.