Abstract
Peritoneal dissemination and growth of tumor cells in the ascitic fluid in stages III and IV of recurrent ovarian cancer is difficult to treat; resistance to many anticancer drugs used in the treatment of solid ovarian cancer is observed at this stage. The author’s hypothesis that the differences in the molecular phenotype of tumor cells for various types of the disease could be an explanation for this. A comparative evaluation of the expression and coexpression of a number of molecular markers (immunofluorescence assay with flow cytometry) was performed using solid and ascitic ovarian cancer cells. In contrast to solid ovarian cancer, ascitic ovarian cancer cells present leukocyte common antigen CD45 and mesenchymal marker vimentin in addition to epithelial marker cytokeratin. In addition to the inhibition of anoikis (specific mechanism of epithelial cell death in a liquid medium in the absence of contact with the substrate), ascitic ovarian cancer cells are characterized by (1) emperipolesis (intracellular migration of leukocytes without damage to the tumor cell), and (2) phenotype of epithelial-mesenchymal transition. Thus, the data on clinically significant molecular differences between solid and recurrent ascitic ovarian cancer was first obtained, opening up opportunities for anticancer therapy, which previously was not used in the treatment of ovarian cancer.
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