Abstract
Cancer surgery is the oldest modality in cancer management and remains an effective cancer treatment that excises visible
tumor and can result in long-lasting clinical cure. Yet the mechanism for the ability of surgery to cure cancer is not understood.
The conventional thinking is that surgery effectively excises all tumor before it spreads and that results in cure. However, with
more recent studies to detect circulating tumor cells that can still persist after tumor excision, it is now increasingly clear that
early tumor spread before clinical detection is a common process of cancer development. Then the important paradoxical
question is how does a local therapy such as surgical excision cure a systemic disease like cancer? We hypothesize that the
interaction between tumor metastasis and antitumor immunity answers this question. The model, which we call “post-surgery
tumor recurrence window model”, suggests that establishment of cancer metastases has an L –shaped kinetics following removal
of the primary tumor. Similarly, pre-surgery concomitant antitumor immunity will also decay following surgery due to lack of
antigen stimulation. Whether a new metastasis can establish is determined by the balance between these two processes. Here
we present animal study evidence to support this model. We also present examples of how this model may be applied to predict
post-surgery prognosis in individual cancer patients.
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