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联合治疗相关摘要翻译样例

发布者:鑫达医学翻译 发布时间:2013-08-24 8:50:52 阅读:

 

原文:

Personalized therapy of advanced non-small cell lung cancer (NSCLC) has been improved by the introduction of EGFR tyrosine kinase inhibitors (TKIs), gefitinib and erlotinib. EGFR TKIs induce dramatic objective responses and increase survival in patients bearing sensitizing mutations in the EGFR intracytoplasmic tyrosine kinase domain. However, virtually all patients develop resistance, and this is responsible for disease relapse. Hence several efforts are being undertaken to understand the mechanisms of resistance in order to develop combination treatments capable to sensitize resistant cells to EGFR TKIs. Recent studies have suggested that upregulation of another member of the EGFR receptor family, namely ErbB3 is involved in drug resistance, through increased phosphorylation of its intracytoplasmic domain and activation of PI3K/AKT signaling. In this paper we first show, by using a set of malignant pleural effusion derived cell cultures (MPEDCC) from patients with lung adenocarcinoma, that surface ErbB3 expression correlates with increased AKT phosphorylation. Antibodies against ErbB3, namely A3, which we previously demonstrated to induce receptor internalization and degradation, inhibit growth and induce apoptosis only in cells overexpressing surface ErbB3. Furthermore, combination of anti-ErbB3 antibodies with EGFR TKIs synergistically affect cell proliferation in vitro, cause cell cycle arrest, up-regulate p21 expression and inhibit tumor growth in mouse xenografts. Importantly, potentiation of gefitinib by anti-ErbB3 antibodies occurs both in de novo and in ab initio resistant cells. Anti-ErbB3 mAbs strongly synergize also with the dual EGFR and HER2 inhibitor lapatinib. Our results suggest that combination treatment with EGFR TKI and antibodies against ErbB3 should be a promising approach to pursue in the clinic.

 

译文:

EGFR酪氨酸激酶抑制剂(TKIs)、吉非替尼和埃罗替尼的使用已经使晚期非小细胞肺癌(NSCLC)的个体化治疗得到改善。在EGFR胞质内酪氨酸激酶结构域发生敏感突变的患者中,EGFR TKIs可引发显著的个体反应,并能增加存活率。 而事实上,所有患者都会形成抗性,从而导致疾病复发。因此,目前多种研究正致力于弄清抗性机制,通过联合疗法消除抗性细胞对EGFR TKIs的抗性。最近研究表明,通过增强胞质内结构域的磷酸化作用和激活PI3K/AKT信号通路,可向上调节EGFR受体家族的另一成员ErbB3,从而形成抗药性。本研究利用肺癌腺癌患者的一系列恶性胸腔积液细胞培养物(MPEDCC)首次指出,表面ErbB3表达与AKT磷酸化作用增强有关。只有当细胞过量表达表面ErbB3时,诱导受体内陷和降解的抗ErbB3抗体(A3)才会抑制生长,诱导凋亡。此外,抗ErbB3抗体与EGFR TKIs联合发挥协同作用,影响体外细胞增殖,在小鼠异种移植物中引起细胞周期停滞,上调p21的表达,抑制肿瘤生长。重要的是,无论是在新形成的抗性细胞中还是在一开始就具有抗性的细胞中,抗ErbB3抗体均可增强吉非替尼的作用。 抗ErbB3突变抗体mAbs也可与EGFR/HER2抑制剂拉帕替尼强烈协同。 我们的结果表明,EGFR TKI与抗ErbB3抗体联合疗法将是临床中追求的理想疗法。


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