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Abstract
The biology of ovarian carcinoma differs from that of hematogenously metastasizing
tumors because ovarian cancer cells primarily disseminate within the peritoneal cavity
and are only superficially invasive. However, since the rapidly proliferating tumors
compress visceral organs and are only temporarily chemosensitive, ovarian carcinoma
is a deadly disease, with a cure rate of only 30%. There are a number of genetic and
epigenetic changes that lead to ovarian carcinoma cell transformation. Ovarian carcinoma
could originate from any of three potential sites: the surfaces of the ovary, the
fallopian tube, or the mesothelium-lined peritoneal cavity. Ovarian cacinoma tumorigenesis
then either progresses along a stepwise mutation process from a slow growing borderline
tumor to a well-differentiated carcinoma (type I) or involves a genetically unstable
high-grade serous carcinoma that metastasizes rapidly (type II). During initial tumorigenesis,
ovarian carcinoma cells undergo an epithelial-to-mesenchymal transition, which involves
a change in cadherin and integrin expression and up-regulation of proteolytic pathways.
Carried by the peritoneal fluid, cancer cell spheroids overcome anoikis and attach
preferentially on the abdominal peritoneum or omentum, where the cancer cells revert
to their epithelial phenotype. The initial steps of metastasis are regulated by a
controlled interaction of adhesion receptors and proteases, and late metastasis is
characterized by the oncogene-driven fast growth of tumor nodules on mesothelium covered
surfaces, causing ascites, bowel obstruction, and tumor cachexia.