Mohindru Mani, Verma Amit
Strategic Analysis Healthcare Inc., Dallas, Texas, USA.
Indian J Pediatr. 2004 Aug;71(8):713-8. doi: 10.1007/BF02730661.
Genetic mutations can lead to abnormal activation of certain kinases that in turn lead to excessive cell division seen in cancers. Inhibitors of over activated kinases can theoretically inhibit cancer causing pathways and result in tumor shrinkage. These discoveries have sparked a revolution in drug discovery with many small molecule kinases inhibitors now being used in cancer clinical trials. The amazing success of Imatinib, a blocker of the bcr-abl kinase in chronic myeloid leukemia has shown that the drugs based on these strategies can improve cure rates in cancer. In this article, the authors review the concepts of kinase inhibition in cancer and principles behind the success of imitanib. The authors also review other promising kinase inhibitors being used in clinical trials that are expected to aid the fight against cancer.
基因突变可导致某些激酶异常激活，进而引发癌症中出现的细胞过度分裂。理论上，过度激活的激酶抑制剂可抑制致癌途径并导致肿瘤缩小。这些发现引发了药物研发的一场革命，如今许多小分子激酶抑制剂正用于癌症临床试验。伊马替尼作为慢性髓性白血病中bcr-abl激酶的阻断剂，其惊人的成功表明基于这些策略的药物可提高癌症治愈率。在本文中，作者回顾了癌症中激酶抑制的概念以及伊马替尼成功背后的原理。作者还回顾了其他正在临床试验中使用的、有望助力抗癌斗争的有前景的激酶抑制剂。
