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Cytogenetic Response in Chronic Myeloid Leukaemia Patients Treated with Imatinib Mesylate Homolog-Drugs:6 Year’s Transitional Study
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作者 Najmaddin Khoshnaw Bassam Francis +2 位作者 Banaz M.Safar Salim S.Mahmood Beston F.Nore 《Journal of Cancer Therapy》 2014年第5期453-459,共7页
Background: Treatment for Chronic Myeloid Leukaemia (CML) is mainly imatinib mesylate (IM) from original-brand, Glivec? or generic-type homologs, Imatib?. Materials and Methods: A collection of 149 CML patients was tr... Background: Treatment for Chronic Myeloid Leukaemia (CML) is mainly imatinib mesylate (IM) from original-brand, Glivec? or generic-type homologs, Imatib?. Materials and Methods: A collection of 149 CML patients was treated over a period of 6 years at Hiwa hospital. These patients were clustered into three groups: Group A was treated with Imatib for more than one year. All survivors of group A patients were switched to Glivec, classified as group B. Group C received only Glivec after June 2011. Imatib and Glivec are administered at doses 400-, 600- and 800-mg according to the CML stage. Results: Among group A patients, 68 (60%) were in complete haematological response (CHR), 32 (28.3%) developed acceleration and 13 (11.5%) patients were deceased. After switching to Glivec (group B), 69 (69%) patients remained in CHR, 10 (10%) patients weredeceased and 21 (21%) patients remained in acceleration. Of the 36 patients in group C, 33 (91.7%) were in CHR, 1 (2.8%) were in acceleration and 2 (5.5%) deceased. Those patients with CHR were tested randomly for BCR/ABL by FISH, and only 1/25 (4%) patients were found with complete cytogenetic response (CCyR) in group A, while 31/42 (73.8%) and 13/17 (76.5%) have CCyR in group B and C, respectively. Conclusions: Our results demonstrate a less cytogenetic response to treatment in patients of CML, who received the Imatib therapy, while a significant cytogenetic remission was found in patients with CHR after they switched to Glivec. 展开更多
关键词 Chronic Myeloid Leukaemia Glivec^(■) Imatib^(■) Complete Haematological Response Cytogenetic Remission
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肌动蛋白在体外与p38激酶结合并抑制其激酶活性 被引量:3
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作者 杨琨 姜勇 +1 位作者 韩家淮 顾军 《中国科学(C辑)》 CSCD 北大核心 2002年第4期346-354,共9页
p38激酶(简称p38)参与炎症、应急、细胞生长与凋亡、细胞周期调控、缺血/再灌损伤及心肌肥厚等生理、病理过程中的信号转导.为了研究该信号通道的分子机理和调节作用,寻找p38的结合蛋白,并检测其相互作用对激酶活性的影响,采用体外蛋... p38激酶(简称p38)参与炎症、应急、细胞生长与凋亡、细胞周期调控、缺血/再灌损伤及心肌肥厚等生理、病理过程中的信号转导.为了研究该信号通道的分子机理和调节作用,寻找p38的结合蛋白,并检测其相互作用对激酶活性的影响,采用体外蛋白结合试验,在细菌内毒素或紫外辐射处理的鼠源性巨噬细胞系(RAW264.7)中,发现有两种蛋白在体外与p38直接结合,其中一种蛋白经肽质谱图鉴定为β-肌动蛋白(β-actin),激酶活性检测表明,actin在体外抑制p38的自磷酸化活性,并抑制p38对其底物ATF2的磷酸化作用.提示actin与p38的结合在体内可能产生一种负反馈作用,调节p38通路的信号转导,从而调节细胞功能. 展开更多
关键词 丝裂原活化蛋白激酶 P38激酶 肌动蛋白 体外蛋白结合 蛋白-蛋白相互作用 信号通道 激酶活性
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