An analysis of 114 patients with dermal melanocytosis on the trunk and extremities.

Dermal melanocytosis is commonly treated with Q-switched neodymium:yttrium-aluminium-garnet (Nd:YAG) laser today. We report on the clinical effect of laser treatment of dermal melanocytosis of the trunk and extremities in 114 patients. The effect of numbers of such treatment was assessed by clinical examination and classified into six grades. All the patients who had more than eight treatments achieved more than 75% clearance. Deep-blue with brown speckled lesions tended to clear more easily than uniform deep-blue lesions. We expect that all dermal melanocytosis of the trunk and extremities can be cleared after a maximum of 12 treatments.

Complete inhibition of human ovarian cancer xenografts in nude mice by suramin and cis-diamminedichloroplatinum(II).

In this study, we have determined the adjuvant effects of suramin to cis-diamminedichloroplatinum(II) (CDDP) on human ovarian cancer (KF) cell growth in vitro and in vivo. Suramin inhibited the ovarian cancer cell proliferation in vitro in a dose-dependent manner between 10 and 80 microM, showing the IC50 of 29 microM. From analysis of flow cytometry (FCM), suramin seemed to be a blocker of G2-M phase of the cell cycle. From the results of the isobologram, suramin appeared to have additive and somewhat synergistic effects on antitumor activity of CDDP. When 5 x 10(5) KF cells were inoculated sc into the right flank of nude mice, 8 of 10 mice formed solid tumor at 4 weeks. When 2 mg/kg CDDP was administered ip every week, the 80% tumor formation was prolonged to 10 weeks. Treatment with 5 and 10 mg/kg suramin decreased the formation rate of palpable tumor to 50 and 30%, respectively. When CDDP was followed by 5 or 10 mg/kg suramin, the tumor formation rate was 20 or 0%. On the other hand, if suramin was followed by CDDP, the tumor formation was not observed in any mouse during the experimental period. These results suggest that suramin may provide a new strategy for treatment of refractory ovarian carcinoma.

[Circumvention of cisplatin resistant ovarian cancer cells by antiestrogens].

Antiestrogens (AEs) have been considered to elicit antitumor effects via estrogen receptor. However, recent reports have demonstrated that AEs had an antitumor effect even in cases without estrogen receptor, and that AEs caused various kinds of biological behavior such as a chemosensitizing effect. We therefore investigated the possibility of circumvention of cisplatin (CDDP) resistance due to the chemosensitizing effect of AEs by using 5 ovarian cancer cell lines. They were named KF, MH, KK, KFra and KFrb cell lines. KF and MH were derived from serous cystadenocarcinomas, and KK from a clear cell carcinoma. KFra and KFrb were CDDP-resistant cell lines developed from the KF cell line. MCF-7 cell line derived from breast cancer was used as a control. The study of a 50% inhibitory concentration (IC50) revealed that clomiphene (CLO) had the most potent antiproliferative effect among the AEs used, and was followed by tamoxifen (TAM) and toremifene (TOR) with a similar effect. On the whole, the degree of CDDP sensitivity was not correlated with the degree of AE sensitivity. KFra cell line which had the highest CDDP-resistance among the 5 ovarian cancer cell lines used was the most sensitive to AEs, especially to CLO. In the study on the combined administration of CDDP and AEs, 1 microM of CLO significantly reduced the IC50 of CDDP to KFrb, KK and MCF-7 cell lines. Similarly, 1 microM of TAM significantly reduced the IC50 of CDDP to KF, KFra and MCF-7 cell lines, and 1 microM of TOR significantly reduced it to KFra, KK and MCF-7 cell lines.(ABSTRACT TRUNCATED AT 250 WORDS)

[Establishment of a cisplatin-resistant human ovarian cancer cell line].

A human ovarian cancer cell line designated "MH" was established from ascites of a patient with ovarian serous cystadenocarcinoma treated with cisplatin. This cell line was grown for more than 2 years and over 100 passages in medium RPMI1640 containing 10% FCS. The cell doubling time, saturation density and plating efficiency was approximately 6.3 days, 5.5 x 10(4)/cm2, and 42%, respectively. Chromosomal analysis revealed aneuploidy with a modal number of 72 and 14-19 types of marker chromosomes. CA125 was detected in both the original tumor and the cultured cells. This cell line is cisplatin-resistant (IC50: 3.28 microM) and has high protein kinase C activity.

[Cytokinetic effects of cisplatin on cisplatin-resistant ovarian cancer cell lines].

Cytokinetic effects of cisplatin on human ovarian cancer cell lines with natural cisplatin-resistance was examined by means of flow cytometry. These ovarian cancer cell lines derived from patients with clear cell carcinoma and serous cystadenocarcinoma were established and designated "KK" and "MH", respectively. Both KK and MH cells have shown resistance to cisplatin and IC50 of them were 0.95 microM and 3.28 microM, respectively. Cisplatin inhibited cell cycle progression at G2 +M phase up to IC50 of each cell from the analysis of cell cycle. Similar results had been obtained in the case of "KF" cell which was sensitive to cisplatin. Further studies of these cells should be performed to elucidate the mechanism of cisplatin resistance.

Total lactate dehydrogenase and its isozymes in serum from patients with primary carcinoma of the ovary.

Serum lactate dehydrogenase (LDH), its isozymes and alpha-hydroxybutyrate dehydrogenase (HBD) were examined in 57 patients with primary carcinoma of the ovary and compared to those in 220 patients with benign ovarian tumor. Serum LDH, LDH-4, LDH-5 and HBD in patients with ovarian carcinoma were significantly higher than those in patients with benign ovarian tumor. Except for the percent fraction of LDH-5, LDH activity, LDH-4 activity, percent fraction of LDH-4, LDH-5 activity and HBD activity in patients with ovarian carcinoma correlated significantly with stage of disease. The positive result of ovarian carcinoma was highest at LDH-4 activity (43.6%), followed by LDH activity (42.1%), HBD activity (34.6%), LDH-5 activity (32.7%), percent fractions of LDH-4 and LDH-5 (20.0%). On the other hand, the false-positive rate in patients with benign ovarian tumor was highest at LDH activity (12.7%), followed by HBD activity (10.0%), LDH-5 activity (8.6%), percent fraction of LDH-5 (8.2%), LDH-4 activity (6.8%) and percent fraction LDH-4 (3.6%). The detection rate for early ovarian carcinoma (stages I and II) was elevated from 4.5% by HBD activity alone to 50.0% by a combination assay of LDH, LDH-4, LDH-5 and HBD, while that for advanced ovarian carcinoma (stages III and IV) was elevated from 50.0% by HBD alone to 79.4% by the combination assay.(ABSTRACT TRUNCATED AT 250 WORDS)