Abstract
The peritoneal metastatic route of cancer dissemination is shared by cancers of the ovary and gastrointestinal tract. Once initiated, peritoneal metastasis typically proceeds rapidly in a feed-forward manner. Several factors contribute to this efficient progression. In peritoneal metastasis, cancer cells exfoliate into the peritoneal fluid and spread locally, transported by peritoneal fluid. Inflammatory cytokines released by tumor and immune cells compromise the protective, anti-adhesive mesothelial cell layer that lines the peritoneal cavity, exposing the underlying extracellular matrix to which cancer cells readily attach. The peritoneum is further rendered receptive to metastatic implantation and growth by myofibroblastic cell behaviors also stimulated by inflammatory cytokines. Individual cancer cells suspended in peritoneal fluid can aggregate to form multicellular spheroids. This cellular arrangement imparts resistance to anoikis, apoptosis, and chemotherapeutics. Emerging evidence indicates that compact spheroid formation is preferentially accomplished by cancer cells with high invasive capacity and contractile behaviors. This review focuses on the pathological alterations to the peritoneum and the properties of cancer cells that in combination drive peritoneal metastasis.
Highlights
Intraperitoneal dissemination is the primary metastatic route of ovarian cancers
This review focuses on the pathological alterations to the peritoneum and the properties of cancer cells that in combination drive peritoneal metastasis
Colorectal, and pancreatic cancer cells bind to mesothelial cell surface receptors ICAM-1 and/or VCAM-1 [28,29,30], which are upregulated in response to injury or insult [25]
Summary
Intraperitoneal dissemination is the primary metastatic route of ovarian cancers. It is a common progression for gastrointestinal malignancies including colorectal, gastric, and pancreatic cancers, for which it signifies a grim prognosis [1, 2]. The poor prognosis relates, in large part, to the rapid progression of peritoneal metastasis in comparison to the hematological (blood-borne) metastatic route This latter route, recently reviewed [3, 4], is a more laborious process that involves cancer cell penetration of multiple barriers during intravasation and extravasation from blood vessels, as well as growth in a foreign environment. Type II EOCs frequently have p53 mutations and are, genetically unstable and present histologically as high-grade serous, mixed epithelial, or undifferentiated carcinomas These cancers are thought to seed the ovarian surface and pelvic peritoneum concurrently, which explains why they rarely present as stage I disease [5]. This review summarizes the current understanding of mechanisms involved in peritoneal metastasis, with a focus on altered cell–cell and cell–matrix dynamics
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