Marked preoperative regression of biopsy-diagnosed microsatellite instability-high colon adenocarcinoma with a small residual traditional serrated adenoma: A case report

Introduction: Marked regression of colorectal cancer before surgery is extremely rare. Microsatellite instability-high (MSI-high) tumors are characterized by a high neoantigen burden and pronounced immunogenicity. Biopsy-associated tissue injury may induce local inflammatory and reparative responses; whether these responses can augment antitumor immunity in an immunogenic tumor microenvironment remains uncertain. We report a case of MSI-high colorectal adenocarcinoma that markedly regressed after biopsy, with no residual carcinoma identified in the resected specimen. The temporal and histopathologic findings raise the possibility of an interplay between biopsy-associated tissue injury and the intrinsic immunogenicity of an MSI-high tumor. Case Report: Initial colonoscopy in a man in his 70s identified an ascending colon lesion consisting of a protruded component and a shallow depressed component. Magnifying endoscopy demonstrated irregular vascular and surface patterns corresponding to Japan NBI Expert Team (JNET) type 2B, together with a type Vi pit pattern, raising suspicion of submucosal invasion. Biopsy specimens obtained from the lesion revealed moderately to well-differentiated adenocarcinoma. Polymerase chain reaction (PCR)-based MSI testing of the biopsy specimen demonstrated MSI-high status. Follow-up colonoscopy performed 36 days later showed regression of the protruded component. Laparoscopic ileocecal resection (LIR) with lymph node dissection was performed 77 days after the initial diagnosis. Macroscopically, only a small protruded lesion measuring approximately 3 mm remained at approximately the same longitudinal level as the tattoo but several centimeters away along the colonic wall. Histopathologic examination revealed a 3-mm traditional serrated adenoma (TSA) with low-grade dysplasia, accompanied by prominent submucosal fibrosis in the presumed tumor bed. No viable adenocarcinoma was identified despite extensive additional sectioning. Moderate lymphocytic infiltration accompanied by lymphoid follicle formation was observed within the presumed tumor bed. Conclusion: Although the underlying mechanism cannot be definitively established, the interval endoscopic regression observed after biopsy and the absence of residual carcinoma in the resected specimen are consistent with a possible regression process. However, complete mechanical removal of the malignant component during biopsy or changes resulting from procedure-related tissue injury cannot be excluded. The MSI-high status and lymphocytic infiltration with lymphoid follicle formation provide a plausible immunologic context, but the contribution of an immune-mediated mechanism remains speculative.