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Despite advances in surgical technique and multimodal therapy, peritoneal carcinomatosis remains the most common and lethal pattern of recurrence in gastric cancer.The persistence of peritoneal disease following apparently curative D2 lymphadenectomy raises the possibility that conventional surgical approaches leave behind residual disease in tissues that appear histologically normal.The concept of field cancerization the replacement of normal cell populations by cancer-primed cells that may show no morphological change is well established in the gastric mucosa and offers a framework for understanding this clinical challenge.Whether a comparable cancerized field exists in the histologically normal peritoneum has not been directly demonstrated, and we treat this as a hypothesis rather than an established finding throughout this review.We examine the biological foundations of field cancerization in gastric cancer, with particular attention to the embryological origins of gastric and peritoneal tissues.We propose, as a novel and testable hypothesis, that the shared embryological origin of gastric mesenchyme and peritoneal mesothelium in the lateral plate mesoderm may help explain the propensity for peritoneal dissemination and the limitations of conventional surgery.We further hypothesize that the extent of lymph node dissection could serve as an indirect indicator of the adequacy of peritoneal field clearance, given the shared embryological background of these compartments.The emerging concept of field dissection is discussed as a conceptual, currently unvalidated extension of curative gastrectomy that would require experimental and prospective clinical evaluation before any clinical application, rather than as an established surgical strategy.
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Cangoz et al. (2026) studied this question.
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