DPYD*6 plays an important role in fluoropyrimidine toxicity in addition to DPYD*2A and c.2846A>T: a comprehensive analysis in 1254 patients.


Journal

The pharmacogenomics journal
ISSN: 1473-1150
Titre abrégé: Pharmacogenomics J
Pays: United States
ID NLM: 101083949

Informations de publication

Date de publication:
12 2019
Historique:
received: 27 03 2018
accepted: 21 12 2018
revised: 30 09 2018
pubmed: 7 2 2019
medline: 2 7 2020
entrez: 7 2 2019
Statut: ppublish

Résumé

Dihydropyrimidine dehydrogenase (DPYD) is a highly polymorphic gene and classic deficient variants (i.e., c.1236G>A/HapB3, c.1679T>G, c.1905+1G>A and c.2846A>T) are characterized by impaired enzyme activity and risk of severe adverse drug reactions (ADRs) in patients treated with fluoropyrimidines. The identification of poor metabolizers by pre-emptive DPYD screening may reduce the rate of ADRs but many patients with wild-type genotype for classic variants may still display ADRs. Therefore, the search for additional DPYD polymorphisms associated with ADRs may improve the safety of treatment with fluoropyrimidines. This study included 1254 patients treated with fluoropyrimidine-containing regimens and divided into cohort 1, which included 982 subjects suffering from gastrointestinal G≥2 and/or hematological G≥3 ADRs, and cohort 2 (control group), which comprised 272 subjects not requiring dose reduction, delay or discontinuation of treatment. Both groups were screened for DPYD variants c.496A>G, c.1236G>A/HapB3, c.1601G>A (DPYD*4), c.1627A>G (DPYD*5), c.1679T>G (DPYD*13), c.1896T>C, c.1905 + 1G>A (DPYD*2A), c.2194G>A (DPYD*6), and c.2846A>T to assess their association with toxicity. Genetic analysis in the two cohorts were done by Real-Time PCR of DNA extracted from 3 ml of whole blood. DPYD c.496A>G, c.1601G>A, c.1627A>G, c.1896T>C, and c.2194G>A variants were found in both cohort 1 and 2, while c.1905+1G>A and c.2846A>T were present only in cohort 1. DPYD c.1679T>G and c.1236G>A/HapB3 were not found. Univariate analysis allowed the selection of c.1905+1G>A, c.2194G>A and c.2846A>T alleles as significantly associated with gastrointestinal and hematological ADRs (p < 0.05), while the c.496A>G variant showed a positive trend of association with neutropenia (p = 0.06). In conclusion, c.2194G>A is associated with clinically-relevant ADRs in addition to the already known c.1905+1G>A and c.2846A>T variants and should be evaluated pre-emptively to reduce the risk of fluoropyrimidine-associated ADRs.

Identifiants

pubmed: 30723313
doi: 10.1038/s41397-019-0077-1
pii: 10.1038/s41397-019-0077-1
pmc: PMC6867961
doi:

Substances chimiques

Pyrimidines 0
Dihydrouracil Dehydrogenase (NADP) EC 1.3.1.2
pyrimidine K8CXK5Q32L

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

556-563

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Auteurs

Marzia Del Re (M)

Clinical Pharmacology and Pharmacogenetics Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

Saverio Cinieri (S)

Medical Oncology Division and Breast Unit, Civil Hospital, Brindisi, Italy.

Angela Michelucci (A)

Medical Genetics Unit, Department of Laboratory Medicine, Azienda Ospedaliero-Universitaria Pisana, Pisa, Italy.

Stefano Salvadori (S)

Epidemiology and Health Services Research Department, Institute of Clinical Physiology, National Research Council (CNR), Pisa, Italy.

Fotios Loupakis (F)

Medical Oncology Unit, Istituto Oncologico del Veneto IRCCS, Padova, Italy.

Marta Schirripa (M)

Medical Oncology Unit, Istituto Oncologico del Veneto IRCCS, Padova, Italy.

Chiara Cremolini (C)

Medical Oncology Unit, Department of Translational Research and New Technologies in Medicine, University of Pisa, Pisa, Italy.

Stefania Crucitta (S)

Clinical Pharmacology and Pharmacogenetics Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

Cecilia Barbara (C)

Medical Oncology Unit, Civil Hospital, Livorno, Italy.

Angelo Di Leo (A)

Medical Oncology Unit, Civil Hospital, Prato, Italy.

Tiziana Pia Latiano (TP)

Medical Oncology Unit, Casa Sollievo della Sofferenza IRCCS, San Giovanni Rotondo, Italy.

Filippo Pietrantonio (F)

Medical Oncology Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy.

Samantha Di Donato (S)

Medical Oncology Unit, Civil Hospital, Prato, Italy.

Paolo Simi (P)

Medical Genetics Unit, Department of Laboratory Medicine, Azienda Ospedaliero-Universitaria Pisana, Pisa, Italy.

Alessandro Passardi (A)

Medical Oncology Unit, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori IRCCS, Meldola, Italy.

Filippo De Braud (F)

Medical Oncology Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy.

Giuseppe Altavilla (G)

Medical Oncology Unit, Department of Human Pathology, University of Messina, Messina, Italy.

Claudio Zamagni (C)

Medical Oncology Unit, Addarii Institute of Oncology, S. Orsola-Malpighi Hospital, Bologna, Italy.

Roberto Bordonaro (R)

Medical Oncology Unit, Department of Oncology, ARNAS Garibaldi, Catania, Italy.

Alfredo Butera (A)

Medical Oncology Unit, Department of Oncology, Civil Hospital, Agrigento, Italy.

Evaristo Maiello (E)

Medical Oncology Unit, Casa Sollievo della Sofferenza IRCCS, San Giovanni Rotondo, Italy.

Carmine Pinto (C)

Medical Oncology Unit, Arcispedale Santa Maria Nuova IRCCS, Reggio Emilia, Italy.

Alfredo Falcone (A)

Medical Oncology Unit, Department of Translational Research and New Technologies in Medicine, University of Pisa, Pisa, Italy.

Valentina Mazzotti (V)

Statistics Applied to Clinical Trials Unit, Azienda Ospedaliero-Universitaria Pisana, Pisa, Italy.

Riccardo Morganti (R)

Statistics Applied to Clinical Trials Unit, Azienda Ospedaliero-Universitaria Pisana, Pisa, Italy.

Romano Danesi (R)

Clinical Pharmacology and Pharmacogenetics Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy. romano.danesi@unipi.it.

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