Peritoneal carcinomatosis: A malignant disease with an embryological origin?

• Transcoelomic spread was described as a main route for PC dissemination.
• Metaplasia of pluripotent stem cells and synchronous malignant transformation, may cause intraperitoneal field cancerization.
• In PC, most serous metastases presented a common embryological origin in the lateral plate of mesoderm.
• Genetic and epigenetic changes, could mark the structures derived from mesoderm, affecting their cell linage descendants.

IntroductionIn 1931, Simpson et al. coined the term “peritoneal carcinomatosis” to describe the regional spread of ovarian tumors as localized or extended with involvement of the peritoneal serous membrane and neighboring anatomical structures.Research into the origin of peritoneal carcinomatosis is based on two phases in a woman's life:Embryo developmentDuring week 3, the bilaminar disc becomes a trilaminar disc called the mesoderm. Inside the lateral plate mesoderm, the coelomic cavity is divided into 2 layers: the parietal (somatic) mesoderm, which gives rise to the parietal peritoneum and pleural surfaces; and the visceral (splanchnic) mesoderm, which gives rise to the visceral peritoneum, visceral surface of the pleura, gonadal stroma, and the muscular layer of the hollow viscera and its mesenteries.Tumor spreadTranscoelomic metastasis and metaplasia of pluripotent stem cells in the peritoneum was involved in the pathogenesis of ovarian cancer. This involvement takes the form of a synchronous malignant transformation at multiple foci and may cause intraperitoneal field cancerization.Pluripotent stem cells play a role both in the development of the embryonic peritoneum and in the spread of transcoelomic tumors. Consequently, knowledge of the origin of these cells (embryonic or current) could be extremely useful.The many markers that act during the embryonic period can affect descendants, that is, cells are already marked before specification and differentiation are activated. Thus, programmed activation could be attributed to genetic and epigenetic changes.