(Originally published in the first issue of the International Journal of Surgery, 2014) As the primary treatment for resectable solid tumors, surgery, while treating the disease, also causes a certain degree of trauma to the body and generates a wide range of pathophysiological and immunological responses, and in the case of progressive tumors, the tumor cells/tissues remaining in the body after resection of the primary focus are invariably subject to certain effects. Very early on, foreign scientists have noted the ability of surgical trauma to affect the biological behavior of tumor tissue, promote tumor dissemination and metastasis, and thus influence the outcome of surgical treatment [1,2]. However, for quite a long time, open surgery has been the main modality of surgical treatment for solid tumors, and advances in surgical techniques have not fundamentally changed this treatment paradigm, and people must suffer from the adverse effects of surgical trauma while treating tumors. Until the last two or three decades, minimally invasive surgical techniques, represented by laparoscopy and robotics, have been applied more and more widely, and the surgical pattern of solid tumors has changed significantly [3]. In this context, it is of great clinical and practical significance to study the effect of surgical trauma on the biological behavior of tumor tissues. Zhang Xiaoqiao, General Surgery Department, General Hospital of Jinan Military Region Surgical treatment inevitably leads to a certain degree of trauma to the organism, especially oncological surgery, which often requires ensuring sufficient resection area of the primary lesion organ and implementing standardized regional lymph node removal in order to completely remove the lesion and achieve R0 resection. However, this principle can also lead to greater trauma, more extensive surgical site injury and significant systemic reactions, all of which may have some effect on the residual tumor lesions in vivo. As early as about 100 years ago, it has been noted that tumor cells have a high affinity for trauma sites, and Rous et al. demonstrated through a series of experiments that peritoneal injury can significantly increase the growth of tumor cells in the peritoneal inoculum, and that the main mechanism of this promotion lies in the proliferation of connective tissue located under the endothelium after mechanical injury, thus forming a stroma that contributes to the growth of tumor tissue [4]. In recent years, some scholars have also applied a rat colpotomy and anastomosis model to demonstrate that, in addition to the wound of dissection, tumor cells inoculated via different routes such as cardiac, abdominal, and colonic lumen after surgery formed tumor nodules involving the entire intestinal wall in the colonic anastomosis, and this effect was most pronounced with inoculation on days 2-8 after surgery, which means that the anastomosis during the healing process can significantly promote tumor cell proliferation [5]. Thus, in this respect, “tumorigenicity” may be considered as one of the intrinsic properties of surgical procedures, as they have so far been accompanied by wound formation [6]. In addition to the effects of local trauma, the resection of the primary lesion will also affect the biological behavior of the tumor cells. Several studies have observed that surgery can inhibit apoptosis and promote tumor cell proliferation in residual lesions in vivo. After surgery, many cytokines, such as tumor necrosis factorα (TNF-α), interleukin-6 (IL-6), and vascular endothelial growth factor (VEGF), whose concentrations in the blood Most of these cytokines can promote the growth of tumor cells or inhibit their apoptosis [7,8]. In addition to the above cytokines, the role of bacterial cell wall components such as lipopolysaccharide (LPS) in promoting perioperative tumor growth has also gained attention in recent years. Studies have shown that surgery itself can induce a certain degree of intestinal bacterial translocation, leading to increased intestinal-derived LPS concentrations in the blood. LPS is not only a potent pro-inflammatory mediator that stimulates the release of many of the aforementioned cytokines, but also has a role in promoting angiogenesis and enhancing tumor cell adhesion [9,10]. Therefore, this series of changes brought about by surgery may disrupt the “balance” between the primary and micro-metastases and activate the dormant tumor cells after resection, which may eventually lead to tumor recurrence [11]. Surgery can also affect the immune status of the body, thus providing an opportunity for the formation of metastases. Under the combined effect of surgical trauma as well as anesthesia and blood transfusion, the post-surgical organism is often in a state of immunosuppression, and the non-specific anti-tumor activity of NK cells and LAK cells is significantly suppressed, and the number of dendritic cells is significantly decreased, thus impairing the overall cellular immune function [12-14]. Although this state of immunosuppression after surgery is transient, lasting only about 1 to 3 weeks, it is sufficient to make the early post-surgical period a window of immunological opportunity favoring the growth and dissemination of tumor cells evading the body’s immune surveillance [6]. In addition to the promotion of tumor metastasis through the local and systemic mechanisms described above, the surgical operation itself may lead to the dissemination of tumor cells. While removing the tumor, the pulling and squeezing of the tumor tissue by the surgical operation; contamination of other sites by surgical instruments with adherent tumor cells also create conditions for the dissemination of tumor cells. The increase of circulating tumor cells in the blood after surgery and the presence of shed cancer cells in the surgical area have been confirmed by several methods [15,16]. Although the clinical significance of the majority of circulating tumor cells and shed cancer cells, which do not ultimately form metastases, remains to be further clarified, these results are sufficient to confirm that surgical manipulation plays a role in promoting tumor cell dissemination. Given the detrimental effects of surgical treatment on the biological behavior of tumors, it is natural to try to adopt means to eliminate or compensate for these defects. In response to the mechanisms listed above, approaches used so far have been non-peripheral intraoperative chemotherapy, immune-enhancing therapy, anti-angiogenic, antioxidant and anti-endotoxic agents application, and biomodulation therapy that attempts to maintain the dormant state of micrometastases, among others. However, since tumor recurrence and metastasis are complex, multifactorial processes involved, it has not been possible so far to evaluate the long-term outcome of these measures, and these ideas to inhibit tumor growth in the perioperative period could not become accepted treatment strategies [6]. However, since surgical trauma is the initiator of these factors and has a pivotal and central role, laparoscopic surgery, with its significant minimally invasive effect, is supposed to have certain oncological advantages that cannot be matched by traditional open surgery. With the increasing application of laparoscopic techniques, in-depth studies on the pathophysiological changes of the body after laparoscopic surgery have been carried out. Although there are still some controversies and conflicting results due to different experimental designs and methodologies, most experimental and clinical studies have shown that the intensity of the systemic inflammatory response of the body after laparoscopic surgery is significantly lower than that of open surgery, which is manifested by a smaller increase in the concentration of acute phase proteins such as C-reactive protein, inflammatory cytokines such as TNF-α and IL-6, and growth factors such as VEGF in the blood. The concentration of γ-interferon γ (IFN-γ), which has an immune enhancing function, is significantly higher than that of open surgery, which is conducive to promoting antigen presentation and maintaining the immune function of the body, so the effect of laparoscopic surgery on the cellular immune function of the body is much less than that of open surgery [17-19]. To date, laparoscopic surgery has mostly been performed using carbon dioxide pneumoperitoneum, avoiding the contact between air and the peritoneal cavity that accompanies open surgery, and studies have shown that this significantly reduces endotoxin translocation, protects peritoneal macrophage function, and attenuates the systemic effects of surgical trauma [9]. In addition, because laparoscopic instruments are more delicate and lighter than conventional open surgical instruments, and can better follow the no touch technique of first cutting off the blood supply to the target organ and separating from the inside out, some studies have shown that the increase in the number of free/circulating cancer cells in the body after laparoscopic surgery is comparable to or significantly lower than that of open surgery. Therefore, laparoscopic surgery does not promote tumor cell dissemination compared to open surgery [20]. Since laparoscopic surgery is superior to open surgery in terms of many of the aforementioned adverse effects of surgical oncology on tumor biological behavior, it is reasonable to expect that laparoscopic surgery would produce better therapeutic outcomes, not just limited to surgical invasiveness indicators such as less trauma and faster recovery, when it is equivalent to open surgery in terms of lymph node clearance and extent of resection of the primary site. To date, there have been a number of clinical studies addressing this issue. While most clinical trials have shown comparable survival benefits for laparoscopic surgery and open surgery, a larger prospective randomized controlled study by Lacy et al. showed a better survival advantage for laparoscopic colon cancer compared to open surgery at a median follow-up of 43 months, mainly in stage III patients, with better tumor recurrence rates and overall survival than open surgery. This advantage persisted when the follow-up period was extended to 95 months. Multifactorial analysis showed that laparoscopic surgery became an independent posterior factor affecting indicators such as tumor recurrence and tumor-related death. This result provides strong evidence that laparoscopic surgery has advantages in surgical oncology, especially in the surgical treatment of progressive tumors, that are unmatched by traditional open surgery due to properties such as better protection of immune function, reduction of stress and inflammatory response, and less harassment of tumor tissue [3,21]. In summary, the application of minimally invasive techniques in surgical oncology is expected to further improve the treatment effect of solid tumors on the one hand, and on the other hand, it also creates conditions for us to deeply understand the influence of surgical trauma on the biological behavior of tumors, thus providing new ideas to improve the treatment effect of tumors. 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