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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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愛(ài)與雨下: 金幣+1 2012-09-25 21:24:07
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當(dāng)前時(shí)代的研究抗血管生成治療癌癥始于1971出版與�？寺母挥邢胂罅Φ募僬f(shuō)，但33年前經(jīng)過(guò)1將第一藥物作為一個(gè)血管生成抑制劑被批準(zhǔn)的食品和藥物管理局（美國(guó)）。2這個(gè)批準(zhǔn)是基于生存受益觀察一3階段隨機(jī)試驗(yàn)的第一線治療轉(zhuǎn)移性結(jié)直腸癌；在審判中，貝伐單抗，一個(gè)人性化的單克隆抗體針對(duì)血管內(nèi)皮生長(zhǎng)因子（血管內(nèi)皮生長(zhǎng)因子），是常規(guī)化療聯(lián)合貝伐單抗治療。4也增加整體生存在第一線治療晚期非小細(xì)胞肺癌的–配合使用時(shí)，與標(biāo)準(zhǔn)化療。5其他抗血管生成的藥物，多吉和舒尼替尼，也被美國(guó)食品和藥物管理局批準(zhǔn)；這些都是小分子受體酪氨酸激酶抑制劑（口服rtkis）。他們的目標(biāo)是多種受體酪氨酸激酶，包括血管內(nèi)皮生長(zhǎng)因子受體和血小板衍生生長(zhǎng)因子（生長(zhǎng)因子）受體。6多吉和舒尼替尼是有益的，在治療轉(zhuǎn)移性腎細(xì)胞癌時(shí)，單獨(dú)使用。7、8多吉單一還活躍在肝癌治療中的carcinoma9和最近批準(zhǔn)了美國(guó)食品和藥物管理局的這一指示。 生存利益的這些治療是相對(duì)溫和（通常以月來(lái)衡量），除了可能的好處患者的腎細(xì)胞癌。這些治療也costly10和有毒副作用。11、12這些問(wèn)題提出以下問(wèn)題方面的改善抗血管生成療法：如何做這樣的工作，以及如何貝伐單抗增加化療的療效？一些理論假設(shè)已，13,14,15,16包括理論，抗血管生成藥物改善化療造成“腫瘤血管正�；保ㄒ�(jiàn)附件1的補(bǔ)充附件，可與全文，本文在www.nejm的。）。如何成為抗腫瘤血管生成的藥物？在臨床上有用的標(biāo)記，可以預(yù)測(cè)效果的這一類藥物？有前途的替代生物標(biāo)志物的藥效學(xué)，將有助于確定最佳劑量特定的代理？將抗rtkis如舒尼替尼或多吉一貫提高化療的療效？賬戶的副作用這些代理商？11 , 12 許多新發(fā)現(xiàn)有可能不僅是為了回答這些問(wèn)題，但也表明新的治療目標(biāo)和治療策略。這次審查的目的是總結(jié)了一些這些發(fā)現(xiàn)，主要是在過(guò)去5年，并指出其潛在的臨床影響。 |
2樓2012-09-25 15:12:45
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