激酶抑制剂用于癌症治疗：我们从伊马替尼中学到了什么？
Cancer treatment with kinase inhibitors: what have we learnt from imatinib?
作者信息
Ross D M, Hughes T P
机构信息
Division of Haematology, Institute of Medical and Veterinary Science, PO Box 14 Rundle Mall, Adelaide SA 5000, Australia.
出版信息
Br J Cancer. 2004 Jan 12;90(1):12-9. doi: 10.1038/sj.bjc.6601507.
Abstract
Over the past few years, a number of anticancer drugs have been developed that specifically target kinases known to be oncogenic. The leading drug in this area is imatinib mesylate, which targets ABL, KIT and PDGFR. It has been remarkably effective in the treatment of chronic myeloid leukaemia, although resistance remains a significant problem. From the imatinib experience in this setting, we present some principles of kinase inhibition that may have more general applicability in targeted anticancer therapy. It is clear that the identification of appropriate targets (activated kinases) and monitoring levels of response (to recognise emerging resistance) are essential to optimise clinical management.
摘要
在过去几年中，已经开发出了多种抗癌药物，这些药物专门针对已知具有致癌性的激酶。该领域的领先药物是甲磺酸伊马替尼，它作用于ABL、KIT和PDGFR。尽管耐药性仍然是一个重大问题，但它在治疗慢性髓性白血病方面非常有效。基于伊马替尼在这种情况下的经验，我们提出了一些激酶抑制的原则，这些原则可能在靶向抗癌治疗中具有更广泛的适用性。很明显，确定合适的靶点（激活的激酶）并监测反应水平（以识别新出现的耐药性）对于优化临床管理至关重要。
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本文引用的文献
1
2
Hypopigmentation in an African patient treated with imatinib mesylate: a case report.
J Natl Med Assoc. 2003 Aug;95(8):722-4.
3
Molecular monitoring of chronic myeloid leukemia.
Semin Hematol. 2003 Apr;40(2 Suppl 2):62-8. doi: 10.1053/shem.2003.50044.
4
A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome.
N Engl J Med. 2003 Mar 27;348(13):1201-14. doi: 10.1056/NEJMoa025217.
5
Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL.
Cell. 2003 Mar 21;112(6):831-43. doi: 10.1016/s0092-8674(03)00190-9.
6
Polycythemia vera responds to imatinib mesylate.
Am J Med Sci. 2003 Mar;325(3):149-52. doi: 10.1097/00000441-200303000-00007.
7
Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia.
N Engl J Med. 2003 Mar 13;348(11):994-1004. doi: 10.1056/NEJMoa022457.
8
Result of high-dose imatinib mesylate in patients with Philadelphia chromosome-positive chronic myeloid leukemia after failure of interferon-alpha.
Blood. 2003 Jul 1;102(1):83-6. doi: 10.1182/blood-2003-01-0025. Epub 2003 Mar 13.
9
Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis.
Blood. 2003 Jul 1;102(1):276-83. doi: 10.1182/blood-2002-09-2896. Epub 2003 Mar 6.
10
MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models.
Blood. 2003 Mar 15;101(6):2368-73. doi: 10.1182/blood.V101.6.2368.
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