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yin198716新虫 (正式写手)
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The current era of research in antiangiogenic therapy for cancer began in earnest in 1971 with the publication of Folkman's imaginative hypothesis,1 but 33 years would elapse before the first drug developed as an inhibitor of angiogenesis was approved by the Food and Drug Administration (FDA).2,3 This approval was based on the survival benefit observed in a randomized phase 3 trial of first-line treatment of metastatic colorectal cancer; in that trial, bevacizumab, a humanized monoclonal antibody directed against vascular endothelial growth factor (VEGF), was combined with conventional chemotherapy.4 Bevacizumab therapy also increased overall survival in the first-line treatment of advanced non–small-cell lung cancer when used in combination with standard chemotherapy.5 Two other antiangiogenic drugs, sorafenib and sunitinib, have also been approved by the FDA; these are oral small-molecule-receptor tyrosine kinase inhibitors (RTKIs). They target multiple receptor tyrosine kinases, including VEGF receptors and platelet-derived growth factor (PDGF) receptors.6 Sorafenib and sunitinib have been beneficial in the treatment of metastatic renal-cell cancer when used alone.7,8 Sorafenib monotherapy is also active in the treatment of hepatocellular carcinoma9 and was recently approved by the FDA for this indication. The survival benefits of these treatments are relatively modest (usually measured in months), with the possible exception of the benefits for patients with renal-cell carcinoma. These treatments are also costly10 and have toxic side effects.11,12 These concerns raise the following questions with respect to improving antiangiogenic therapy: How do such drugs work, and how does bevacizumab increase the efficacy of chemotherapy? Several theories have been postulated,13,14,15,16 including the theory that antiangiogenic drugs improve chemotherapy by causing "vessel normalization" in tumors (see Appendix 1 of the Supplementary Appendix, available with the full text of this article at www.nejm.org). How do tumors become resistant to antiangiogenic drugs? Are there clinically useful markers that can predict the efficacy of this class of drug? Are there promising surrogate pharmacodynamic biomarkers that will help to determine the best dose of a particular agent? Will antiangiogenic RTKIs such as sunitinib or sorafenib consistently enhance the efficacy of chemotherapy? What accounts for the side effects of these agents?11,12 Many recent discoveries have the potential not only to answer some of these questions but also to indicate new therapeutic targets and treatment strategies. The purpose of this review is to summarize a number of these discoveries, made mainly over the past 5 years, and to point out their potential clinical impact. |
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【答案】应助回帖
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爱与雨下: 金币+1 2012-09-25 21:24:07
phu_grassman: 金币+2, bonus for your time and energy. 2012-10-30 17:58:53
sltmac: 金币+5 2012-11-24 10:57:09
sltmac: 翻译EPI+1, 欢迎常来~~ 2012-11-24 10:57:17
爱与雨下: 金币+1 2012-09-25 21:24:07
phu_grassman: 金币+2, bonus for your time and energy. 2012-10-30 17:58:53
sltmac: 金币+5 2012-11-24 10:57:09
sltmac: 翻译EPI+1, 欢迎常来~~ 2012-11-24 10:57:17
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当前时代的研究抗血管生成治疗癌症始于1971出版与福克曼的富有想象力的假说，但33年前经过1将第一药物作为一个血管生成抑制剂被批准的食品和药物管理局（美国）。2这个批准是基于生存受益观察一3阶段随机试验的第一线治疗转移性结直肠癌；在审判中，贝伐单抗，一个人性化的单克隆抗体针对血管内皮生长因子（血管内皮生长因子），是常规化疗联合贝伐单抗治疗。4也增加整体生存在第一线治疗晚期非小细胞肺癌的–配合使用时，与标准化疗。5其他抗血管生成的药物，多吉和舒尼替尼，也被美国食品和药物管理局批准；这些都是小分子受体酪氨酸激酶抑制剂（口服rtkis）。他们的目标是多种受体酪氨酸激酶，包括血管内皮生长因子受体和血小板衍生生长因子（生长因子）受体。6多吉和舒尼替尼是有益的，在治疗转移性肾细胞癌时，单独使用。7、8多吉单一还活跃在肝癌治疗中的carcinoma9和最近批准了美国食品和药物管理局的这一指示。 生存利益的这些治疗是相对温和（通常以月来衡量），除了可能的好处患者的肾细胞癌。这些治疗也costly10和有毒副作用。11、12这些问题提出以下问题方面的改善抗血管生成疗法：如何做这样的工作，以及如何贝伐单抗增加化疗的疗效？一些理论假设已，13,14,15,16包括理论，抗血管生成药物改善化疗造成“肿瘤血管正常化”（见附件1的补充附件，可与全文，本文在www.nejm的。）。如何成为抗肿瘤血管生成的药物？在临床上有用的标记，可以预测效果的这一类药物？有前途的替代生物标志物的药效学，将有助于确定最佳剂量特定的代理？将抗rtkis如舒尼替尼或多吉一贯提高化疗的疗效？账户的副作用这些代理商？11 , 12 许多新发现有可能不仅是为了回答这些问题，但也表明新的治疗目标和治疗策略。这次审查的目的是总结了一些这些发现，主要是在过去5年，并指出其潜在的临床影响。 |
2楼2012-09-25 15:12:45
yin198716
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3楼2012-10-30 14:01:00
