Letrozole as well as progestins could be the first choice of treatment for patients with recurrent or residual LGESS, which is difficult to resect surgically because of its efficacy and minimal adverse effects.

A two-tier system in which ovarian epithelial carcinomas are subdivided into type I and type II tumors has been proposed on the basis of recent molecular pathogenesis findings. Type I tumors, unrelated to tumor protein p53 (TP53) mutations, show favorable prognosis in a slow step-wise process, whereas type II tumors, related to TP53 mutations, contribute to poor prognosis. Ovarian serous carcinomas with excessive psammoma bodies behave like type I tumors. However, their etiology and prognostic significance remain obscure. The objective of the present study was to evaluate the characteristic features and potential relevance of psammoma bodies to the clinical outcome of 44 patients with serous carcinomas with long-term follow-up. The 5-and 10-year survival rates were significantly different between the serous carcinomas with less than 5% area of psammoma bodies and those at least 5% area (P < 0.01). All tumors with at least 5% area were both diploid and immunohistochemically negative for TP53 mutations. All patients with these tumors, including eight with International Federation of Gynecology and Obstetrics (FIGO) stages III or IV disease, survived more than 5 years and their 10-year survival rate was 76%. In multivariate analysis using clinical parameters, the apparent existence of psammoma bodies was an indication to view serous carcinomas as type I tumors with long-term survival. Our results suggested that the formation of psammoma bodies is associated with increased apoptotic tumor cell death related to normal TP53 function. The pathological findings of psammoma bodies might contribute to the consideration of pathogenesis and to the development of prognostic prediction rules for serous carcinomas. (Cancer Sci 2010; 101: 1550-1556 O varian carcinoma is the fifth leading cause of cancerrelated death and the most lethal malignancy of the female reproductive tract.(1) The clinical outcome of patients with advanced ovarian carcinoma is poor despite aggressive surgery and intensive chemotherapy. Accurate evaluation of the primary tumor is important to determine the prognosis and treatment strategies. Various known prognostic factors such as clinical stage of disease, histological grade, and DNA ploidy have been established in an effort to estimate a patient's individual prognosis and to improve therapeutic strategies in ovarian carcinoma. (2)(3)(4)(5) Shih and Kurman recently proposed a model of ovarian carcinogenesis based on clinical, pathological, and molecular genetic studies.(6) The model divides ovarian carcinomas into two groups designated type I and type II. Type I tumors show favorable prognosis and generally develop from wellestablished precursor lesions or borderline tumors. Type I tumors, including micropapillary serous carcinoma (7) and well-differentiated serous carcinoma, are genetically stable and are characterized by mutations in a number of different genes including v-Ki-ras2 kirsten rat sarcoma viral oncogene homolog (KRAS), v-raf murine sarcoma viral oncogene homolog B1 (BRAF), and v-erb-b2 ery...

No abstract

No abstract