Ovarian Cancer Stroma: Pathophysiology and the Roles in Cancer Development
AbstractOvarian cancer represents one of the cancers with the worst prognostic in adult women. More than half of the patients who present with clinical signs such as abdominal bloating and a feeling of fullness already show advanced stages. The majority of ovarian cancers grow as cystic masses, and cancer cells easily spread into the pelvic cavity once the cysts rupture or leak. When the ovarian cancer cells disseminate into the peritoneal cavity, metastatic nests may grow in the cul-de-sac, and in more advanced stages, the peritoneal surfaces of the upper abdomen become the next largest soil for cancer progression. Ascites is also produced frequently in ovarian cancers, which facilitates distant metastasis. Clinicopathologic, epidemiologic and molecular studies on ovarian cancers have improved our understanding and therapeutic approaches, but still further efforts are required to reduce the risks in the patients who are predisposed to this lethal disease and the mortality of the patients in advanced stages. Among various molecules involved in ovarian carcinogenesis, special genes such as TP53, BRCA1 and BRCA2 have been well investigated. These genes are widely accepted as the predisposing factors that trigger malignant transformation of the epithelial cells of the ovary. In addition, adnexal inflammatory conditions such as chronic salpingitis and ovarian endometriosis have been great research interests in the context of carcinogenic background of ovarian cancers. In this review, I discuss the roles of stromal cells and inflammatory factors in the carcinogenesis and progression of ovarian cancers. View Full-Text
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Furuya, M. Ovarian Cancer Stroma: Pathophysiology and the Roles in Cancer Development. Cancers 2012, 4, 701-724.
Furuya M. Ovarian Cancer Stroma: Pathophysiology and the Roles in Cancer Development. Cancers. 2012; 4(3):701-724.Chicago/Turabian Style
Furuya, Mitsuko. 2012. "Ovarian Cancer Stroma: Pathophysiology and the Roles in Cancer Development." Cancers 4, no. 3: 701-724.