药物治疗抵抗在临床实践中成为肿瘤治疗失败的主因。最近的研究指出,肿瘤细胞的耐药性可能源于其内部高度的细胞异质性,而这种异质性的基础则是肿瘤可塑性。肿瘤细胞可塑性可能引发一系列反应,包括对治疗的耐药性发展、免疫系统逃逸以及对周围组织和血管系统的侵袭和转移等。本文简要介绍肿瘤细胞可塑性的表现形式以及其在药物治疗抵抗的非遗传适应性机制与靶向治疗新策略。

Drug therapy resistance has emerged as a primary cause of treatment failure in cancer management．Recent research indicates that the resistance of tumor cells may stem from their high degree of intracellular heterogeneity,with the underlying basis being tumor plasticity．Tumor cell plasticity can trigger a cascade of responses,including the development of resistance to treatment,evasion of the immune system,and invasion and metastasis into surrounding tissues and the vascular system．This article provides a brief overview of the manifestations of tumor cell plasticity and its non-genetic adaptive mechanisms in drug therapy resistance,along with novel strategies for targeted treatment．

目的 研究罗哌卡因阻滞用于胸腹腔镜联合食管癌根治术后镇痛的临床效果。方法 胸腹腔镜联合食管癌根治术患者60例,分为: 观察组(n=30),缝合切口时用0.25%盐酸罗哌卡因10 mL于切口局部浸润;对照组(n=30) 不做局部浸润麻醉处理;记录二组术后2 h、6 h、12 h、24 h、48 h的疼痛视觉模拟评分(VAS)及血浆皮质醇浓度。结果 观察组术后2 h、6 h、12 h VAS评分优于对照组,术后12 h观察组血浆皮质醇浓度低于对照组。结论 罗哌卡因术终阻滞术后12 h内镇痛效果明显。

Objective To evaluate the efficiency of postoperative analgesia with ropivacaine block after thoracoscopic-lapacoscopic esophagectomy (TLE). Methods Totally 60 patients with esophageal cancer underwent TLE were divided into two groups: observation group(n=30)with 0.25% ropivacaine hydrochloride solution 10 mL injection around incision before end of the operation; control group(n=30)without the treatment. The VAS and the plasma Cortisol concentration at 2 h、6 h、12 h、24 h、48 h after surgery were recorded. Results The VAS at 2 h、6 h、12 h after surgery in observation group was higher than that of the control group,but not at 24 h、48 h after surgery. The plasma Cortisol concentration in the observation group was higher than that of in the control at 12 hours postoperatively. Conclusion Ropivacaine block of incision is helpful to have analgesic effect within 12 hours after TLE.