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Imatinab mesylate treatment in Chronic Myeloid Leukemia (CML)- understanding the fundamental pharmacokinetic and pharmacogenetic mechanisms for variation in response

Although lmatinib mesylate (IM) is the gold standard drug for Chronic Myeloid Leukemia (CML) treatment, resistance to IM emerges in a significant number of patients. Resistance could be due to several factors. Pharmacokinetic variability as a result of genetic polymorphisms in IM metabolizing gen...

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Main Author: Ankathil, Ravindran
Format: Monograph
Language:English
Published: Pusat Pengajian Sains Perubatan, Universiti Sains Malaysia 2016
Subjects:
RC254-282 Neoplasms. Tumors. Oncology (including Cancer)
Online Access:http://eprints.usm.my/58151/1/PROF%20DR%20RAVINDRAN%20ANKATHIL-Eprints.pdf
http://eprints.usm.my/58151/
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spelling my.usm.eprints.58151 http://eprints.usm.my/58151/ Imatinab mesylate treatment in Chronic Myeloid Leukemia (CML)- understanding the fundamental pharmacokinetic and pharmacogenetic mechanisms for variation in response Ankathil, Ravindran RC254-282 Neoplasms. Tumors. Oncology (including Cancer) Although lmatinib mesylate (IM) is the gold standard drug for Chronic Myeloid Leukemia (CML) treatment, resistance to IM emerges in a significant number of patients. Resistance could be due to several factors. Pharmacokinetic variability as a result of genetic polymorphisms in IM metabolizing genes could be a potential factor. This study was undertaken to investigate the genotype frequencies and the impact of ORM1 520G>A, PXR 1792A>G, CAR 540C>T, CYP3A4 878T>C and CYP3A5 6986A>G polymorphisms towards CML susceptibility risk and IM response. A total of 540 subjects (270 CML patients and 250 normal healthy controls) have been recruited in this study. Genotyping was performed and the association between allelic variants and CML susceptibility risk and response to IM treatment were assessed by means of odds ratio (OR) with 95% confident interval s calculated by logistic regression. Results showed that PXR 1792A>G, CAR 540C>T and CYP3A5 6986A>G were significantly associated with IM responses and CAR 540C>T, CYP3A4 878T>C and CYP3A5 6986A>G were significantly associated with CML susceptibility risk. Further study should be done on a larger scale to validate whether this polymorphism can be used as a predictive biomarker for identifying resistance development among CML patients undergoing IM treatment. Pusat Pengajian Sains Perubatan, Universiti Sains Malaysia 2016 Monograph NonPeerReviewed application/pdf en http://eprints.usm.my/58151/1/PROF%20DR%20RAVINDRAN%20ANKATHIL-Eprints.pdf Ankathil, Ravindran (2016) Imatinab mesylate treatment in Chronic Myeloid Leukemia (CML)- understanding the fundamental pharmacokinetic and pharmacogenetic mechanisms for variation in response. Project Report. Pusat Pengajian Sains Perubatan, Universiti Sains Malaysia. (Submitted)
institution Universiti Sains Malaysia
building Hamzah Sendut Library
collection Institutional Repository
continent Asia
country Malaysia
content_provider Universiti Sains Malaysia
content_source USM Institutional Repository
url_provider http://eprints.usm.my/
language English
topic RC254-282 Neoplasms. Tumors. Oncology (including Cancer)
spellingShingle RC254-282 Neoplasms. Tumors. Oncology (including Cancer)
Ankathil, Ravindran
Imatinab mesylate treatment in Chronic Myeloid Leukemia (CML)- understanding the fundamental pharmacokinetic and pharmacogenetic mechanisms for variation in response
description Although lmatinib mesylate (IM) is the gold standard drug for Chronic Myeloid Leukemia (CML) treatment, resistance to IM emerges in a significant number of patients. Resistance could be due to several factors. Pharmacokinetic variability as a result of genetic polymorphisms in IM metabolizing genes could be a potential factor. This study was undertaken to investigate the genotype frequencies and the impact of ORM1 520G>A, PXR 1792A>G, CAR 540C>T, CYP3A4 878T>C and CYP3A5 6986A>G polymorphisms towards CML susceptibility risk and IM response. A total of 540 subjects (270 CML patients and 250 normal healthy controls) have been recruited in this study. Genotyping was performed and the association between allelic variants and CML susceptibility risk and response to IM treatment were assessed by means of odds ratio (OR) with 95% confident interval s calculated by logistic regression. Results showed that PXR 1792A>G, CAR 540C>T and CYP3A5 6986A>G were significantly associated with IM responses and CAR 540C>T, CYP3A4 878T>C and CYP3A5 6986A>G were significantly associated with CML susceptibility risk. Further study should be done on a larger scale to validate whether this polymorphism can be used as a predictive biomarker for identifying resistance development among CML patients undergoing IM treatment.
format Monograph
author Ankathil, Ravindran
author_facet Ankathil, Ravindran
author_sort Ankathil, Ravindran
title Imatinab mesylate treatment in Chronic Myeloid Leukemia (CML)- understanding the fundamental pharmacokinetic and pharmacogenetic mechanisms for variation in response
title_short Imatinab mesylate treatment in Chronic Myeloid Leukemia (CML)- understanding the fundamental pharmacokinetic and pharmacogenetic mechanisms for variation in response
title_full Imatinab mesylate treatment in Chronic Myeloid Leukemia (CML)- understanding the fundamental pharmacokinetic and pharmacogenetic mechanisms for variation in response
title_fullStr Imatinab mesylate treatment in Chronic Myeloid Leukemia (CML)- understanding the fundamental pharmacokinetic and pharmacogenetic mechanisms for variation in response
title_full_unstemmed Imatinab mesylate treatment in Chronic Myeloid Leukemia (CML)- understanding the fundamental pharmacokinetic and pharmacogenetic mechanisms for variation in response
title_sort imatinab mesylate treatment in chronic myeloid leukemia (cml)- understanding the fundamental pharmacokinetic and pharmacogenetic mechanisms for variation in response
publisher Pusat Pengajian Sains Perubatan, Universiti Sains Malaysia
publishDate 2016
url http://eprints.usm.my/58151/1/PROF%20DR%20RAVINDRAN%20ANKATHIL-Eprints.pdf
http://eprints.usm.my/58151/
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score 13.211869

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