Surgical resection represents a cornerstone of cancer treatment. However, clinical observations indicate that tumor recurrence often occurs after surgery [1], which does not necessarily reflect surgical failure. Studies suggest that metastasis may already be present during the early stages of cancer progression, although most metastatic deposits remain dormant and do not expand significantly. As a result, these occult micrometastases are often undetectable by current clinical diagnostic methods [2], [3], [4]. Following tumor resection, such micrometastases can become activated. This phenomenon also accounts for the clinically observed bimodal pattern of postoperative recurrence across various cancer types [5], [6], [7]. In contrast to the single recurrence peak observed in untreated cases, the second peak is generally attributed to natural disease progression, whereas the first peak may be associated with the removal of the primary tumor [8], [9]. Current explanations for this clinical pattern primarily focus on factors related to “surgical manipulation” such as mechanisms involving surgical stress responses and wound healing processes that may accelerate the proliferation of micrometastases [10], [11]. However, another variable is the “primary tumor site” and the removal of the primary tumor disrupts the complex dynamic equilibrium between the primary site and the body's antitumor response.

In 1908, Bashford introduced the concept of concomitant immunity (CI), which describes an antitumor immune response triggered by the presence of the primary tumor. Although this response is insufficient to affect the primary site, it can suppress the progression of metastatic lesions [12]. Clinical observations suggest that preoperative CI—likely sustained by the primary tumor as the main source of tumor antigens—may restrain micrometastases, inducing a dormant state. However, surgical removal of the primary tumor leads to the abrupt loss of this primary antigen source, thereby impairing the ability of CI to control micrometastases. The underlying mechanism for the loss of CI following surgery is multifaceted. It involves not only the removal of antigenic stimulation but also the impact of the surgical procedure itself on immune function. Thus, the surgical intervention and the elimination of the primary tumor are not independent events; rather, they interact synergistically to promote tumor recurrence.

Given the rapid advances in tumor immunotherapy in recent years, CI is of vital importance in preventing and treating postoperative recurrence and metastasis. A thorough review of the current theoretical framework surrounding CI is therefore warranted. This paper begins by tracing the evolution of CI theory, reviewing its clinical evidence, mechanisms of action, and ongoing debates. Furthermore, we examine the impact of surgery on CI and outline potential therapeutic strategies grounded in its core principles. The objective is to establish a theoretical foundation for fundamental research on CI and to inform the development of novel strategies to prevent postoperative recurrence and metastasis.