%0 Journal Article
%T Tratamiento con imatinib y el farmacogenotipo CYP3A4 en relaci¨®n con la expansi¨®n clonal Ph(+) en leucemia mieloide cr¨®nica (LMC)
%A Camargo
%A Mauricio
%A Soto-Mar¨ªn
%A Mar¨ªa Isabel
%A Zea
%A Olga
%A Saavedra
%A Domingo
%J Colombia M¨¦dica
%D 2008
%I Scientific Electronic Library Online
%X introduction: imatinib is an inhibitor of the bcr-abl tyrosine-kinase that has dramatically changed the treatment of patient with chronic myeloid leukemia (cml) positive for the philadelphia chromosome (ph+). this compound is mainly metabolized by the cytochrome cyp3a4 enzyme, coded by a gene with individual variations that could interfere with the effectiveness of the treatment, due to the fact that particular single nucleotide polymorphisms (snps), i.e., cyp3a4*1b y cyp3a4*2, have shown to exert a significant influence on the metabolic activity of this pharmacologically important enzyme. objective: evaluate the frequency of pharmacogenetically important polymorphisms in the cyp3a4 gen in a colombian population of patients with cml being treated with this novel drug (imatinib), in parallel with a control population of 164 healthy individuals. correlate the evolution of the clonal expansion ph(+) with the presence of these snps and the length of treatment. methodology: pcr-rflp genotyping for the cyp3a4* 1b y cyp3a4*2 snps. rbhg replication banding for the evaluation of the presence of the ph(+) markers in spontaneous mitotic blasts. results: a positive cytogenetic response and/or correlation was detected between the length of the imatinib treatment and a reduction in the percentage of ph(+) blasts. genotyping indicate that cyp3a4*1b polymorphism does no affect the cytogenetic response in imatinib treated ph(+) patients, and that the pharmacorelevant cyp3a4*2 snp is not present in this population of patients and controls (n=194). conclusions: the pharmacogenotype cyp3a4*2 (exon 7) does not affect the induced positive cytogenetic response triggered by the imatinib treatment, that generally induces a reduction in ph(+) blasts en relation with the duration of the treatment.
%K imatinib
%K chronic myeloid leucemia
%K cml
%K cyp3a4
%K philadelphia chromosome
%K pharmacogenetics
%K snps.
%U http://www.scielo.org.co/scielo.php?script=sci_abstract&pid=S1657-95342008000400003&lng=en&nrm=iso&tlng=en