Pharmacokinetics of imatinib mesylate in end stage renal disease. A case study
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Imatinib Mesylate
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Objective:This study is to investigate the effect of imatinib mesylate on advanced the gastrointestinal stromal tumors(GISTs) and the relationship of curative effect and clinic pathological features.Methods:After treated by imatinib mesylate with starting doses of 400mg/day,the clinic pathological data of 36 advanced gastrointestinal stromal tumors patients were analyzed retrospectively.The patients were divided into different subgroups.Then the short-term effect of Imatinib mesylate among different subgroups and treatment adverse were detected.Results:The recent response rate of patients with Imatinib mesylate was 19 cases(52.8%),and the RR with different metastatic sites(P=0.048) were significantly different.The treatment adverse: edema 20 cases(55.6%),nausea 17 cases(47.2%),and vomit 8 cases(22.2%).And all adverse reactions can be controlled well.Conclusions:Imatinib mesylate has good effect on advanced gastrointestinal stromal tumor.The efficacy is closely related with the metastatic sites.
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The BCR-ABL fusion gene product is a constitutively activated tyrosine kinase, which is fundamental in the pathogenesis of chronic myeloid leukemia (CML). Imatinib mesylate (imatinib, Glivec® or Gleevec®), a small molecule inhibitor of the BCR-ABL tyrosine kinase, is now the first-line treatment for all newly diagnosed chronic phase CML patients. Imatinib treatment results in a high frequency of complete cytogenetic response (CCgR). Patients in CCgR can be further stratified by the degree of minimal residual disease, measured by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). The present thesis deals with different aspects on molecular monitoring of imatinib treated CML patients. By serially analyzing peripheral blood and bone marrow BCR-ABL transcript levels using qRT-PCR in CML patients commencing imatinib therapy, we found that the major decline in BCR-ABL transcripts occurred within 6 months after start of imatinib treatment. An apparent plateau in BCR-ABL transcript level seems to have been reached after 12-15 months of imatinib treatment, which indicates a stable number of remaining BCR-ABL positive cells. To search for markers associated with molecular response in CML patients treated with imatinib, we studied the mRNA expression of apoptosis-related genes in peripheral blood nucleated cells from chronic phase CML patients commencing imatinib treatment. We found that a lower BAD expression at diagnosis correlates with a better molecular response at 12 months of imatinib therapy. Studies of BCR-ABL kinase domain mutations in imatinib treated CML patients revealed that point mutations were mainly associated with acquired resistance, but not with cytogenetic or molecular disease persistence in CML patients without signs of increasing leukemia burden. Finally we studied “off-target” effects of imatinib on peripheral blood on T-lymphocytes. We found that therapeutic doses of imatinib alter the expression of apoptosis related genes in CD3+ lymphocytes and change the phenotype of CD4+CD28+ T-helper cells.
Imatinib Mesylate
Chronic myelogenous leukemia
ABL
breakpoint cluster region
Minimal Residual Disease
Philadelphia chromosome
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Chronic myelogenous leukemia
Imatinib Mesylate
Philadelphia chromosome
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OBJECTIVE To establish a selective isolation method of imatinib mesylate using molecular imprinting technology.METHODS The molecular imprinted polymer(MIP) was synthesized by bulk polymerization using imatinib mesylate as the template.The MIP was investigated for its recognition of imatinib mesylate by equilibrium absorption and solid-phase extraction.RESULTS The MIP had specific absorbability to Imatinib mesylate.CONCLUSION The MIP prepared in the study can be used for selective recognition and isolation of imatinib mesylate analogues from natural products.
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Molecularly imprinted polymer
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Objective To investigate the role of Imatinib mesylate on inhibition of normal human epidermal melanocyte(NHEM) migration.Methods The growth and the differentiation of NHEM were observed by MTT assay.Invasion-chamber was applied to determine the ability of NHEM's migration.Finally phosphorylation of c-kit in NHEM was studied by western blot.Results When the concentrations of Imatinib mesylate in culture medium were reach to 0.1 μmol/L,1.0 μmol/L and 5.0 μmol/L respectively,Imatinib mesylate inhibited NHEM migration that was induced by SCF and Imatinib mesylate also inhibited phosphorylation of c-kit in NHEM.Conclusion Imatinib mesylate can inhibit NHEM migration that was induced by SCF and Imatinib mesylate can also inhibit phosphorylation of c-kit in NHEM.This suggests that Imatinib mesylate may be potential used for prevention of nevus spilus recurrence.
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Abstract Chronic neutrophilic leukemia (CNL) is a rare hematologic disorder, for which there is no standard therapy. Recently, STI (imatinib mesylate) has been shown to be effective in treating patients with chronic myeloproliferative disorder (CMPD) displaying the translocation of the PDGFβR gene. Here, we present a case of a patient with CNL carrying t(15;19)(q13;p13.3) who achieved a cytogenetic remission following treatment with imatinib, 400 mg daily. After failure of alpha interferon and hydroxyurea therapy, a durable and complete clinical and cytogenic remission was induced by imatinib. To our knowledge, this is the first case with CNL who showed complete response with cytogenic remission after treatment of imatinib. The mechanism of response to this molecule is unknown in our case (other oncogenes than c‐kit, tyrosine kinase, or PDGFR may be involved). The patient remains in complete remission with an excellent performance status after 7 months of therapy. We demonstrate here that imatinib can induce a clinical and cytogenetic response in a case of CNL associated with a novel translocation other than a 5q33 rearrangement. Further studies including the molecular cloning of the t(15;19)(q13;p13.3) will be important in understanding the pathophysiology of CNL with a heterogeneous clinical course and the exploitation of the basic mechanisms of imatinib treatment. Am. J. Hematol. 77:366–369, 2004. © 2004 Wiley‐Liss, Inc.
Imatinib Mesylate
Philadelphia chromosome
breakpoint cluster region
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Imatinib Mesylate
Mesylate
Chronic myelogenous leukemia
Hematology
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Imatinib Mesylate
Targeted Therapy
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瞄准：评估并且描绘疾病前进的模式，并且决定胃肠的基质肿瘤(大意) 与 imatinib mesylate 对待的 unresectable 与疾病前进联系了的预示的意义变形或。方法：临床的数据和计算断层摄影术(CT ) 想象回顾地在从 2002 年 10 月与 imatinib mesylate 被对待到 2006 年 10 月的 17 个大意病人被考察。除了为肿瘤反应的评估使用尺寸测量[在稳固的肿瘤(石柜) 标准的反应评估标准] ， CT 变化的模式在治疗期间被评估并且与临床的数据相关。结果：有八非应答者和九个应答者。CT 变化的五个模式在治疗期间被发现：焦点的前进(FP ) ，概括前进(GP ) ，概括膀胱的变化(GC ) ，新膀胱的损害(NC ) 和新稳固的损害(NS ) 。在学习的结束，所有非应答者显示出 GP，而应答者根据石柜标准显示出膀胱的变化(GC 和 NC ) 和反应。全面幸存与 GP 病人相比在 RECIST 标准以内在有膀胱的变化或反应的病人显著地更好(P = 0.0271 ) 。结论：在对 imatinib mesylate 作出回应的有大意的病人的 CT 变化的各种各样的模式被示威，并且可能决定疾病的预后。CT 的标准和模式改变的石柜的联合在大意为反应评估被建议。
Imatinib Mesylate
Mesylate
Stromal tumor
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