Evidence map›Paper›PMID 32047295›Full record

ReviewBritish journal of cancer2020

Emerging roles for UDP-glucuronosyltransferases in drug resistance and cancer progression.

Eric P Allain, Michèle Rouleau, Eric Lévesque, Chantal Guillemette

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
18.4field-weighted citation impact, top 1% 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

88 citing papers in PubMed, 170 citations in OpenAlex.

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  16. Nuclear MBL-1 modulates mitochondrial morphology through carnitine palmitoyltransferase inProceedings of the National Academy of Sciences of the United States of America · 2026
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28 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Eric P Allain *Pharmacogenomics Laboratory, Centre Hospitalier Universitaire (CHU) de Québec Research Center-Laval University, Québec, QC, Canada.
Michèle Rouleau *Pharmacogenomics Laboratory, Centre Hospitalier Universitaire (CHU) de Québec Research Center-Laval University, Québec, QC, Canada.
Eric LévesquePharmacogenomics Laboratory, Centre Hospitalier Universitaire (CHU) de Québec Research Center-Laval University, Québec, QC, Canada.
Chantal GuillemettePharmacogenomics Laboratory, Centre Hospitalier Universitaire (CHU) de Québec Research Center-Laval University, Québec, QC, Canada. chantal.guillemette@crchudequebec.ulaval.ca.
Université Laval · CACentre hospitalier universitaire de Québec · CA

Funding

CIHR FRN#408093Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada) FRN#142318Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada) FRN#152986Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada) FRN#42392
6 · The paper itself

Abstract

The best-known role of UDP-glucuronosyltransferase enzymes (UGTs) in cancer is the metabolic inactivation of drug therapies. By conjugating glucuronic acid to lipophilic drugs, UGTs impair the biological activity and enhance the water solubility of these agents, driving their elimination. Multiple clinical observations support an expanding role for UGTs as modulators of the drug response and in mediating drug resistance in numerous cancer types. However, accumulating evidence also suggests an influence of the UGT pathway on cancer progression. Dysregulation of the expression and activity of UGTs has been associated with the progression of several cancers, arguing for UGTs as possible mediators of oncogenic pathways and/or disease accelerators in a drug-naive context. The consequences of altered UGT activity on tumour biology are incompletely understood. They might be associated with perturbed levels of bioactive endogenous metabolites such as steroids and bioactive lipids that are inactivated by UGTs or through non-enzymatic mechanisms, thereby eliciting oncogenic signalling cascades. This review highlights the evidence supporting dual roles for the UGT pathway, affecting cancer progression and drug resistance. Pharmacogenomic testing of UGT profiles in patients and the development of therapeutic options that impair UGT actions could provide useful prognostic and predictive biomarkers and enhance the efficacy of anti-cancer drugs.

Indexed as

Antineoplastic AgentsDrug Resistance, NeoplasmGlucuronosyltransferaseHumansNeoplasmsSignal TransductionUridine DiphosphateAntineoplastic AgentsGlucuronosyltransferaseUridine Diphosphate

Identifiers

PMID32047295
PMCPMC7188667
OpenAlexW3006091015

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.