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首页> 外文期刊>Expert opinion on biological therapy >Optimizing treatment of metastatic colorectal cancer patients with anti-EGFR antibodies: overcoming the mechanisms of cancer cell resistance.
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Optimizing treatment of metastatic colorectal cancer patients with anti-EGFR antibodies: overcoming the mechanisms of cancer cell resistance.

机译：用抗EGFR抗体优化转移性结直肠癌患者的治疗：克服癌细胞耐药的机制。

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INTRODUCTION: A number of anti-EGFR monoclonal antibodies (mAbs) have been recently developed for the treatment of refractory metastatic colorectal cancer (mCRC). These mAbs, blocking ligand/receptor interactions, exert their biological activity via multiple mechanisms, including inhibition of cell cycle progression, potentiation of cell apoptosis, inhibition of angiogenesis, tumor cell invasion and metastasis and, potentially, induction of immunological effector mechanisms. AREAS COVERED: Cetuximab is an anti-EGFR mAb currently used in mCRC treatment. Despite the evidence of efficacy of cetuximab in the treatment of mCRC patients, the observation of low response rates was the proof of concept of resistance to anti-EGFR mAbs treatment. An increasing number of molecular alterations have been more recently hypothesized to be involved in resistance to anti-EGFR mAbs in CRC: mutations in BRAF, NRAS and PIK3CA, loss of expression of PTEN and, now, activation of HER2 signaling through HER2 gene amplification and/or increased heregulin stimulation. EXPERT OPINION: This review focuses on the development of new strategies such as combination with other agents blocking alternative escape pathways, cancer cell prioritization hyperactivating EGFR pathway, combination with immune system, development of nanotech devices to increase efficacy of antibody-based therapy and overcome the mechanisms of cancer cell resistance.
机译：引言：最近已开发出许多抗EGFR单克隆抗体（mAb），用于治疗难治性转移性结直肠癌（mCRC）。这些阻断配体/受体相互作用的mAb通过多种机制发挥其生物学活性，包括抑制细胞周期进程，增强细胞凋亡，抑制血管生成，肿瘤细胞侵袭和转移以及潜在地诱导免疫效应机制。覆盖的区域：西妥昔单抗是目前用于mCRC治疗的抗EGFR mAb。尽管有西妥昔单抗治疗mCRC患者的疗效的证据，但观察到低应答率仍是抗EGFR mAb治疗耐药概念的证明。最近，越来越多的分子变化被认为与CRC中抗EGFR mAb的抗性有关：BRAF，NRAS和PIK3CA的突变，PTEN表达的丧失以及现在通过HER2基因扩增和激活HER2信号转导。 /或调蛋白刺激增强。专家意见：这篇综述着重于新策略的开发，例如与其他阻断替代逃逸途径的药物联用，癌细胞优先处理的超活化EGFR通路，与免疫系统联用，纳米技术设备的开发，以提高基于抗体的疗法的功效并克服癌细胞抗性的机制。

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