Ovarian cancer is a deadly disease with a low cure rate of only 30%, primarily due to its rapid progression and limited treatment options. The biology of ovarian cancer differs from hematogenously metastasizing tumors, as it primarily spreads within the peritoneal cavity and is only superficially invasive. Ovarian cancer can originate from the ovary, fallopian tube, or peritoneal cavity, and progresses through a stepwise mutation process or involves genetically unstable high-grade serous carcinomas. The epithelial-to-mesenchymal transition (EMT) is a critical step in the initial tumorigenesis, allowing cancer cells to detach from the primary tumor and attach to the abdominal peritoneum or omentum. Metastasis is regulated by adhesion receptors and proteases, with late metastasis characterized by rapid growth of tumor nodules on mesothelium-covered surfaces, leading to ascites, bowel obstruction, and tumor cachexia. The American Cancer Society reported 21,550 cases of epithelial ovarian carcinoma and 14,600 deaths in 2009, making it the gynecologic malignancy with the highest case-to-fatality ratio. High-grade serous carcinomas are the most common type, often originating from the fallopian tube or peritoneal cavity. Treatment strategies for advanced ovarian cancer include aggressive surgery and chemotherapy, with intraperitoneal administration of platinum and taxane showing improved survival compared to intravenous administration. Genetic insights into ovarian carcinoma development suggest two main subtypes: low-grade serous-papillary, endometrioid, and borderline tumors (type I) and high-grade serous carcinomas (type II). Type I cancers are characterized by BRAF, KRAS, and microsatellite instability, while type II cancers are associated with p53 mutations and alterations in the AKT/ phosphatidylinositol 3-kinase pathway. The unique biological behavior of ovarian cancer allows for metastasis through passive mechanisms, carried by peritoneal fluid. EMT and the loss of E-cadherin are crucial for the detachment and invasion of cancer cells. The mesothelium, covering all organs within the peritoneal cavity, serves as the primary microenvironment for ovarian cancer metastasis. Integrins, CD44, and transglutaminase are key proteins involved in adhesion and invasion. Late metastasis involves the formation of new blood vessels to support tumor growth, with VEGF/VEGFR pathways playing a significant role. Microarray studies have shown that primary and metastatic tumors have similar genetic alterations, suggesting that metastasis may not be as complex as in other cancers. Ovarian cancer is a rare disease, presenting limited opportunities for large phase III trials. New treatments should be characterized through translational studies and innovative clinical trial designs. The confined nature of ovarian cancer within the peritoneal cavityOvarian cancer is a deadly disease with a low cure rate of only 30%, primarily due to its rapid progression and limited treatment options. The biology of ovarian cancer differs from hematogenously metastasizing tumors, as it primarily spreads within the peritoneal cavity and is only superficially invasive. Ovarian cancer can originate from the ovary, fallopian tube, or peritoneal cavity, and progresses through a stepwise mutation process or involves genetically unstable high-grade serous carcinomas. The epithelial-to-mesenchymal transition (EMT) is a critical step in the initial tumorigenesis, allowing cancer cells to detach from the primary tumor and attach to the abdominal peritoneum or omentum. Metastasis is regulated by adhesion receptors and proteases, with late metastasis characterized by rapid growth of tumor nodules on mesothelium-covered surfaces, leading to ascites, bowel obstruction, and tumor cachexia. The American Cancer Society reported 21,550 cases of epithelial ovarian carcinoma and 14,600 deaths in 2009, making it the gynecologic malignancy with the highest case-to-fatality ratio. High-grade serous carcinomas are the most common type, often originating from the fallopian tube or peritoneal cavity. Treatment strategies for advanced ovarian cancer include aggressive surgery and chemotherapy, with intraperitoneal administration of platinum and taxane showing improved survival compared to intravenous administration. Genetic insights into ovarian carcinoma development suggest two main subtypes: low-grade serous-papillary, endometrioid, and borderline tumors (type I) and high-grade serous carcinomas (type II). Type I cancers are characterized by BRAF, KRAS, and microsatellite instability, while type II cancers are associated with p53 mutations and alterations in the AKT/ phosphatidylinositol 3-kinase pathway. The unique biological behavior of ovarian cancer allows for metastasis through passive mechanisms, carried by peritoneal fluid. EMT and the loss of E-cadherin are crucial for the detachment and invasion of cancer cells. The mesothelium, covering all organs within the peritoneal cavity, serves as the primary microenvironment for ovarian cancer metastasis. Integrins, CD44, and transglutaminase are key proteins involved in adhesion and invasion. Late metastasis involves the formation of new blood vessels to support tumor growth, with VEGF/VEGFR pathways playing a significant role. Microarray studies have shown that primary and metastatic tumors have similar genetic alterations, suggesting that metastasis may not be as complex as in other cancers. Ovarian cancer is a rare disease, presenting limited opportunities for large phase III trials. New treatments should be characterized through translational studies and innovative clinical trial designs. The confined nature of ovarian cancer within the peritoneal cavity