[Show abstract][Hide abstract] ABSTRACT: Drug resistance is a major concern in the successful treatment of ovarian cancer. In the present study we report a combinational drug regime using arsenic trioxide (ATO) and cisplatin (CDDP) to increase therapeutic potentiality in ovarian cancer cells. ATO-mediated growth inhibition and apoptosis in human suspension ovarian cancer COC1 cells were evaluated by MTT assay and annexin V assay using flow cytometry, respectively. cDNA arrays were performed to screen ATO-mediated gene expression. Treatment of COC1 cells with ATO alone resulted in growth inhibition and apoptosis with a dose-and time-dependent fashion; further cDNA arrays showed that 34 genes (23 up-regulated genes and 11 down-regulated genes) may strongly associate with the antiproliferative and pro-apoptotic effects induced by ATO. Furthermore, Chou-Talalay analysis was used to evaluate the combinational effect of ATO and CDDP as well as dose-reduction index (DRI) in a panel of ovarian cancer cells including CDDP-sensitive and -resistant cell lines. The combination index (CI) analysis indicated that the interaction effect of ATO/CDDP exhibited a wide range of synergism in all the adherent ovarian cancer cells (A2780, IGROV-1, SKOV-3, and R182) as well as 0.93 to 0.69 for IC(50) to IC(90) in suspension COC1 cells where CI < 1, =1, and >1, define synergism, additive effect, and antagonism, respectively. More intriguingly, the combination of ATO and CDDP yielded favorable DRIs ranging from 1.23-fold to 13.51-fold dose reduction. These results suggest that ATO and its combination with CDDP present therapeutic potential for ovarian cancer, and deserve further preclinical and clinical studies.
Cancer Science 09/2009; 100(12):2459-64. DOI:10.1111/j.1349-7006.2009.01340.x · 3.53 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: ObjectiveTo investigate the clinical symptom, ultrasonographic scan finding, serum CA125 value, histopathological type and treatment
of small ovarian tumor (<5 cm) in postmenopausal women.
MethodsRetrospective 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.
ResultsThere 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.
ConclusionSmall 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.
Chinese Journal of Cancer Research 08/2006; 18(3):229-234. DOI:10.1007/s11670-006-0229-0 · 2.16 Impact Factor