Eggermont A M, Steller E P, Sugarbaker P H
Surgery. 1987 Jul;102(1):71-8.
The interrelationship between host resistance to cancer and the trauma of a surgical procedure is the subject of much speculation. Extensive study of animal models and human subjects is required to define these effects and to provide a theoretical model by which to interpret these data. We used a murine model of intraperitoneal cancer to demonstrate the augmentation of tumor growth by surgical trauma. In this intraperitoneal tumor model, a surgical procedure that included entry into the abdominal cavity resulted in augmented tumor growth; a surgical incision on the skin of the animal's back did not promote tumor growth. The immunotherapeutic effects of interleukin-2 and lymphokine-activated killer cells were significantly reduced by the performance of a laparotomy. This abrogation of the effects of the immunotherapeutic regimen was observed for up to 14 days after laparotomy but was lost by days 35 to 42. Healing tissue may promote tumor growth, and these effects are dominant over immunotherapy with interleukin-2 plus lymphokine-activated killer cells.
宿主对癌症的抵抗力与外科手术创伤之间的相互关系是诸多猜测的主题。需要对动物模型和人类受试者进行广泛研究，以确定这些影响，并提供一个理论模型来解释这些数据。我们使用了一种腹膜内癌症的小鼠模型来证明手术创伤会促进肿瘤生长。在这个腹膜内肿瘤模型中，包括进入腹腔的手术操作导致肿瘤生长加速；在动物背部皮肤做一个手术切口则不会促进肿瘤生长。剖腹手术显著降低了白细胞介素-2和淋巴因子激活的杀伤细胞的免疫治疗效果。剖腹手术后长达14天可观察到免疫治疗方案效果的这种消除，但在第35至42天时消失。愈合组织可能促进肿瘤生长，且这些影响比白细胞介素-2加淋巴因子激活的杀伤细胞的免疫治疗更为显著。
