نتایج جستجو برای: the c3435t mdr1 polymorphism

تعداد نتایج: 16069836  

Journal: :middle east journal of cancer 0
yaya kassogue genetics and molecular pathology laboratory, medical school of casablanca, hassan ii university, casablanca, morocco hind dehbi genetics and molecular pathology laboratory, medical school of casablanca, hassan ii university, casablanca, morocco meryem quachouh department of onco-hematology, ibn rochd university hospital, casablanca, morocco asma quessar department of onco-hematology, ibn rochd university hospital, casablanca, morocco said benchekroun department of onco-hematology, ibn rochd university hospital, casablanca, morocco sellama nadifi genetics and molecular pathology laboratory, medical school of casablanca, hassan ii university, casablanca, morocco

background: despite the impressive results obtained with imatinib, inadequate response or resistance are observed in certain patients. it is known that imatinib is a substrate of a multidrug resistance gene (mdr1). thus, interindividual genetic differences linked to single nucleotide polymorphisms in mdr1 may influence the metabolism of imatinib. the present study has aimed to examine the impac...

2013
Jian Gao

The multidrug resistance 1 gene (MDR1) is an important candidate gene for influencing susceptibility to hepatocellular carcinoma (HCC). The objective of the present study was to evaluate the association of MDR1 polymorphisms with the risk of HCC in the Chinese Han population. A total of 353 HCC patients and 335 healthy subjects were enrolled in the study. Polymerase chain reaction-restriction f...

2013
Dan Zhang Cun Wang Zongguang Zhou

OBJECTIVE Many studies have focused on the association between the ABCB1 3435C>T polymorphism and colorectal cancer (CRC) risk. However, the results were conflicting. The aim of this meta-analysis is to evaluate the precise association between this polymorphism and CRC risk. METHODS We formally reviewed the literature at Pubmed, EMBASE and the Cochrane Library with the key words as follows: A...

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