New advances in DPYD genotype and risk of severe toxicity under capecitabine.
Fiche publication
Date publication
janvier 2017
Journal
PloS one
Auteurs
Membres identifiés du Cancéropôle Est :
Dr CHAIGNEAU Loïc, Dr FERRAND Christophe, Pr MERLIN Jean-Louis, Pr PIVOT Xavier
Tous les auteurs :
Etienne-Grimaldi MC, Boyer JC, Beroud C, Mbatchi L, van Kuilenburg A, Bobin-Dubigeon C, Thomas F, Chatelut E, Merlin JL, Pinguet F, Ferrand C, Meijer J, Evrard A, Llorca L, Romieu G, Follana P, Bachelot T, Chaigneau L, Pivot X, Dieras V, Largillier R, Mousseau M, Goncalves A, Roché H, Bonneterre J, Servent V, Dohollou N, Château Y, Chamorey E, Desvignes JP, Salgado D, Ferrero JM, Milano G
Lien Pubmed
Résumé
Deficiency in dihydropyrimidine dehydrogenase (DPD) enzyme is the main cause of severe and lethal fluoropyrimidine-related toxicity. Various approaches have been developed for DPD-deficiency screening, including DPYD genotyping and phenotyping. The goal of this prospective observational study was to perform exhaustive exome DPYD sequencing and to examine relationships between DPYD variants and toxicity in advanced breast cancer patients receiving capecitabine.
Mots clés
Adult, Aged, Antimetabolites, Antineoplastic, adverse effects, Breast Neoplasms, drug therapy, Capecitabine, adverse effects, Dihydrouracil Dehydrogenase (NADP), genetics, Female, Genotype, Humans, Middle Aged, Polymorphism, Single Nucleotide, Prospective Studies
Référence
PLoS ONE. 2017 ;12(5):e0175998