ArticleBritish journal of cancer2020
UGT2B17 modifies drug response in chronic lymphocytic leukaemia.
Article 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 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Roles of Uridine Diphosphoglucuronosyltransferase 2B Enzymes in Cancer Susceptibility and Treatment: A Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Cellular pharmacology of fludarabine: molecular determinants of transport and metabolism.Frontiers in pharmacology · 2026Review
- Role and mechanism of Roux-en-Y gastric bypass in the treatment of diabetic urinary bladder hyperactivity by reducing TRPV1 and P2X3.World journal of diabetes · 2025Article
- The liver proteome of individuals with a natural UGT2B17 complete deficiency.Scientific reports · 2025Article
- Targeting sphingolipid metabolism in chronic lymphocytic leukemia.Clinical and experimental medicine · 2024Article
- Non-canonical transcriptional regulation of the poor prognostic factor UGT2B17 in chronic lymphocytic leukemic and normal B cells.BMC cancer · 2024Article
- Cancer chemoresistance and its mechanisms: Associated molecular factors and its regulatory role.Medical oncology (Northwood, London, England) · 2023Review
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- The Uridine diphosphate (UDP)-glycosyltransferases (UGTs) superfamily: the role in tumor cell metabolism.Frontiers in oncology · 2022Review
- The expression of Phase II drug-metabolizing enzymes in human B-lymphoblastoid TK6 cells.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2022Article
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Authors and funding
21 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundHigh UGT2B17 is associated with poor prognosis in untreated chronic lymphocytic leukaemia (CLL) patients and its expression is induced in non-responders to fludarabine-containing regimens. We examined whether UGT2B17, the predominant lymphoid glucuronosyltransferase, affects leukaemic drug response and is involved in the metabolic inactivation of anti-leukaemic agents.
methodsFunctional enzymatic assays and patients' plasma samples were analysed by mass-spectrometry to evaluate drug inactivation by UGT2B17. Cytotoxicity assays and RNA sequencing were used to assess drug response and transcriptome changes associated with high UGT2B17 levels.
resultsHigh UGT2B17 in B-cell models led to reduced sensitivity to fludarabine, ibrutinib and idelalisib. UGT2B17 expression in leukaemic cells involved a non-canonical promoter and was induced by short-term treatment with these anti-leukaemics. Glucuronides of both fludarabine and ibrutinib were detected in CLL patients on respective treatment, however UGT2B17 conjugated fludarabine but not ibrutinib. AMP-activated protein kinase emerges as a pathway associated with high UGT2B17 in fludarabine-treated patients and drug-treated cell models. The expression changes linked to UGT2B17 exposed nuclear factor kappa B as a key regulatory hub.
conclusionsData imply that UGT2B17 represents a mechanism altering drug response in CLL through direct inactivation but would also involve additional mechanisms for drugs not inactivated by UGT2B17.
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