Abstract
Colorectal cancer remains an important cause of mortality worldwide. The presence of peritoneal carcinomatosis (PC) causes significant symptoms and is notoriously difficult to treat. Therefore, informative preclinical research into the mechanisms and possible novel treatment options of colorectal PC is essential in order to improve the prognostic outlook in these patients. Several syngeneic and xenograft animal models of colorectal PC were established, studying a wide range of experimental procedures and substances. Regrettably, more sophisticated models such as those giving rise to spontaneous PC or involving genetically engineered mice are lacking. Here, we provide an overview of all reported colorectal PC animal models and briefly discuss their use, strengths, and limitations.
Highlights
With an annual worldwide mortality rate of over half a million, colorectal cancer (CRC) remains a major cause of cancer related mortality [1]
Colorectal peritoneal metastasis remains little studied in preclinical models, when compared to ovarian cancer or liver metastasis research
Standardized, reproducible syngeneic and xenograft colorectal peritoneal carcinomatosis (PC) models are available in rodents
Summary
With an annual worldwide mortality rate of over half a million, colorectal cancer (CRC) remains a major cause of cancer related mortality [1]. Since malignant disease causes death by distant organ invasion, the unravelling of molecular mechanisms underlying hematogenous and lymphatic metastasis is a topic of intensive research activity [2]. The introduction of targeted biological agents has met with considerable survival prolongation in patients with metastatic disease [3]. Intraperitoneally located tumors may be at the origin of locoregional peritoneal spread. Often coexisting with systemic disease, it is increasingly realised that colorectal tumor dissemination within the peritoneal cavity may represent a separate phenotypic and molecular entity. Established peritoneal carcinomatosis (PC) from CRC is much less responsive to systemic therapy and causes considerable morbidity in affected patients.
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