Objective: To investigate the clinical symptom, ultrasonographic scan finding, serum CA125 value, histopathological type and treatment of small ovarian tumor (<5 cm) in postmenopausal women. Methods: Retrospective analysis was carried out for 52 clinical materials of ovarian tumor cases in women more than one year after menopausal between Jan 1997 and Dec 2004. The largest diameter of the ovarian mass is less than 5 cm. Results: There were 11 ovarian cancers and 1 borderline ovarian tumor among 52 small ovarian tumors (23.1%). 10 ovarian cancers were epithelial neoplasms and 2 were sex cord-stromal tumors, and 8 cases were in late stage according to FIGO staging system (33.3%). Compared with benign tumor, there is no significant difference in the onset age, interval after menopausal and duration of history. The main clinical feature is abdominal symptoms, such as abdominal pain and distension in the malignant cases. The patients with benign tumors often showed the ovarian mass during the annual screening or admitted into hospital for other causes. The ultrasonography finding and serum CA125 level showed much difference between benign and malignant cases. Unilocular smooth-walled ovarian cysts mostly were found in benign tumor and the CA125 values were always less than 35 U/ml; but the solid or complex sonographic structures (multilocular, or with a papillary projections on the wall) often indicated a high risk of cancer, especially there was ascites in the pelvic cavity. Serum CA125 level in many cancer cases was elevated (>35 U/ml), over 300 U/ml in more than half of the patients. Surgery is still the first choice to treat ovarian cancer, and chemotherapy would be an auxiliary method. Till now, 3 ovarian cancer patients died of complications of cancer and 2 cases had recurrence. Conclusion: Small ovarian tumor in postmenopausal women has a comparatively low malignant occurrence but more in later stage. Many are epithelial carcinoma. If there is complex or parenchymal sonographic structure accompanied with a high serum CA125 level, operation should be considered, while it can be followed up when the ultrasound shows a smooth cyst with normal CA125 value.

Over-expression of EGFR, as in most cases of ovarian cancer, is associated with advanced-stage disease and poor prognosis. Activation of EGFR signaling pathway is involved in increased cell proliferation, angiogenesis, metastasis and decreased apoptosis. Tyrosine kinase activity is essential for signal transduction and receptor down-regulation. However, we found in this study that tyrosine kinase activity is not necessary in ligand-induced EGFR down-regulation in ovarian cancer cell line CaOV3 cells. EGFR tyrosine kinase inhibitors, such as PD153035, AG1478, as well as non-specific tyrosine kinase inhibitor PP2 cannot reverse EGF-induced down-regulation of EGFR. These findings thus permit us to develop the following exciting but unconventional strategy to sensitize cancer cells, namely, by priming ovarian cancer cells with EGF and EGFR inhibitor PD153035, before chemotherapy. This priming procedure down-regulates EGFR without induction of mitogenic signals such as ERK and PI3K/AKT. EGF plus EGFR inhibitor-primed ovarian cancer cells display increased sensitivity to taxol-induced cell death, resistant to EGF-induced cell migration and cell proliferation as well as ERK and PI3K/AKT activation. Further studies showed that PD153035, which does not reverse ligand-induced EGFR down-regulation, blocks EGF-induced EGFR activation as well as EGFR’s binding to c-cbl and Grb2. Taken together, we contend that priming with EGFR inhibitors plus EGF inhibits cell signaling pathways leading to cell proliferation and survival, while down-regulating EGFR. This priming approach sensitizes ovarian cancer cells and would ultimately result in better chemotherapeutical outcome.