Quintuplet pregnancy and third degree ovarian hyperstimulation despite withholding human chorionic gonadotrophin.

A patient who suffered from polycystic ovarian disease and anovulation, was treated with pure follicle stimulating hormone for induction of ovulation. The treatment was stopped and human chorionic gonadotrophin was not administered because of high serum oestradiol levels and multiple follicular development. Ovulation occurred 11 days after pure follicle stimulating hormone was discontinued, the patient developed third-degree ovarian hyperstimulation syndrome and conceived with a quintuplet pregnancy.     

Suppression of human ovarian carcinoma metastasis by the metastasis-suppressor gene, BRMS1

Metastasis-suppressor genes, by definition, suppress metastasis without affecting tumorigenicity and, hence, present attractive targets as prognostic or therapeutic markers. BRMS1 (breast cancer metastasis suppressor) has recently been identified as a metastasis-suppressor gene for human breast cancer and melanoma. Expression of BRMS1 messenger RNA (mRNA) in multitissue including normal prostate, ovarian, testis, and colon has been detected by northern blot analysis. We hypothesize that the role of BRMS1 in tumor progression may not be limited to breast cancer and melanoma. We previously found that BRMS1 mRNA levels in primary ovarian epithelial carcinomas were significantly lower than that in normal ovarian and benign tumors (P < 0.05), and statistical analysis of BRMS1 mRNA levels revealed that BRMS1 mRNA levels were significantly higher in early tumor stages (I, II) compared with advanced tumor stages (III, IV) in which lymph node or distant metastases were present (P < 0.01). Our data showed that reduced BRMS1 mRNA seems to influence ovarian carcinoma metastatic ability. Therefore, we transfected BRMS1 plasmid into highly malignant ovarian carcinoma cell line, HO-8910PM, and examined cell biologic behaviors including proliferation, adhesion, invasion, and metastasis in vitro and in vivo. BRMS1 expression did not alter the proliferation of HO-8910PM cells in vitro and primary tumor formation in vivo. But, BRMS1 expression significantly suppressed the cell adhesion to extracellular matrix components and in vitro cell invasion in BRMS1-transfected HO-8910PM cells compared to parental HO-8910PM and vector-only transfectants (HO-8910PM-vect). Furthermore, motility of BRMS1 transfectants was inhibited. lung colony formation of intravenously injected BRMS1 transfectants in nude mice was significantly reduced. Also, BRMS1 transfectants form significantly less metastatic to organs of peritoneal cavity in orthotopically implanted ovarian tumor nude models. We further discovered that BRMS1 expression did downregulate expression of an actin-bundling protein associated with cell motility -fascin, which perhaps is the mechanism underlying BRMS1 suppression of metastasis. These data suggested that in addition to its already described role in breast cancer and melanoma, BRMS1 functions as a metastasis-suppressor gene in ovarian carcinoma by modifying several metastatic-associated phenotypes, offering a new target for therapeutic intervention.     

Identification of genes associated with ovarian cancer metastasis using microarray expression analysis

Although the transition from early- to advanced-stage ovarian cancer is a critical determinant of survival, little is known about the molecular underpinnings of ovarian metastasis. We hypothesize that microarray analysis of global gene expression patterns in primary ovarian cancer and metastatic omental implants can identify genes that underlie the metastatic process in epithelial ovarian cancer. We utilized Affymetrix U95Av2 microarrays to characterize the molecular alterations that underlie omental metastasis from 47 epithelial ovarian cancer samples collected from multiple sites in 20 patients undergoing primary surgical cytoreduction for advanced-stage (IIIC/IV) serous ovarian cancer. Fifty-six genes demonstrated differential expression between ovarian and omental samples (P < 0.01), and twenty of these 56 differentially expressed genes have previously been implicated in metastasis, cell motility, or cytoskeletal function. Ten of the 56 genes are involved in p53 gene pathways. A Bayesian statistical tree analysis was used to identify a 27-gene expression pattern that could accurately predict the site of tumor (ovary versus omentum). This predictive model was evaluated using an external data set. Nine of the 27 predictive genes have previously been shown to be involved in oncogenesis and/or metastasis, and 10/27 genes have been implicated in p53 pathways. Microarray findings were validated by real-time quantitative PCR. We conclude that gene expression patterns that distinguish omental metastasis from primary epithelial ovarian cancer can be identified and that many of the genes have functions that are biologically consistent with a role in oncogenesis, metastasis, and p53 gene networks.     

Primary peritoneal carcinoma in a UK cancer center: comparison with advanced ovarian carcinoma over a 5-year period

Abstract.   Jaaback KS, Ludeman L, Clayton NL, Hirschowitz L. Primary peritoneal carcinoma in a UK cancer center: comparison with advanced ovarian carcinoma over a 5-year period. Int J Gynecol Cancer 2006; 16(Suppl. 1): 123–128.
The relative incidence of primary peritoneal carcinoma (PPCa) and advanced (FIGO stage III or IV) ovarian serous carcinoma (AOSCa) was assessed over 5 years at a UK cancer center, and the sociodemographic, clinical, and survival data were compared. There were 23 women with PPCa and 55 with AOSCa. The ratio of PPCa:AOSCa was higher than previously reported. No statistical difference was found between the two groups with regard to age (mean 64.43 vs 64.07 years, P = 0.9), parity (1.6 vs 1.8, P = 1.0), personal/family history of another malignancy (although five patients with AOSCa but none with PPCa had personal histories of breast cancer), or serum CA125, CA19.9, and carcinoembryonic antigen (CEA) levels. Similar numbers in both groups had malignant ascites, although 5.8% of patients with AOSCa but none with PPCa had negative cytology. Tumor grade, stage, treatment, and survival were similar (median 586 vs 641 days, P = 0.66). This analysis of the largest published UK series of patients with PPCa does not support previous reports that patients with PPCa are older than those with AOSCa and have a worse prognosis; it suggests that both groups have similar sociodemographic characteristics, clinical profiles, and survival.     

Arsenic trioxide exposure to ovarian carcinoma cells leads to decreased level of topoisomerase II and cytotoxicity

The objective of this study was to investigate the effect of arsenic trioxide (As(2)O(3)) on topoisomerase II levels using western blotting method on MDAH 2774 ovarian carcinoma cell culture. Experimental designs were established to determine the cytotoxic effects of As(2)O(3) on MDAH 2774 cells and the IC50 (fatal dose for the 50% of cells) value. Cytotoxicity experiments were carried out using various concentrations of As(2)O(3). The 2,3-bis[2-methyloxy-4-nitro-5-sulfophenyl]-2H-tetrazolium-5-carboxanilide (XTT) and trypan blue dye-exclusion tests were used to evaluate cytotoxicity. Topoisomerase II expressions were investigated using western blotting method with various concentrations of As(2)O(3). Densitometric analysis of topoisomerase 2 bands was carried out using Quantity One 1-D analysis software (Bio-Rad USA, Life Science Research, Hercules, CA). IC50 value of As(2)O(3) was found to be 5 x 10(-6) M for MDAH 2774 cells. When the bands were evaluated, it was observed that there was a decrease in topoisomerase II levels in MDAH 2774 cells with increasing concentrations of As(2)O(3). It was also observed by the densitometric analysis that topoisomerase II expression ratios of MDAH 2774 cells were decreased by approximately 50% at this concentration. Topoisomerase II levels were significantly decreased with the increasing concentrations of As(2)O(3). Inhibition of topoisomerase II enzyme was one of the antiproliferative influence mechanisms of As(2)O(3).     

老年糖尿病患者冠状动脉血流储备变化的初步观察

目的　应用彩色多普勒超声仪检测冠状动脉血流储备 (coronaryflowreserve ,CFR) ,初步观察老年糖尿病患者中CFR的变化。方法　 2 5例老年糖尿病患者及 2 5例健康志愿者作对照组 ,比较两组的空腹血糖 (FBG)、早餐后 2h血糖 (P2hBG)、糖化血红蛋白A1c (HbA1c)、总胆固醇 (TC)、低密度脂蛋白胆固醇 (LDL C)及甘油三酯(TG)、内皮素 1(ET 1)、静息状态时患者冠状动脉的基础血流速度 (bFV)、潘生丁注射后的最大冠脉血流速度(mFV)及CFR。结果　糖尿病组的FBG、P2hBG、TG及ET 1水平显著高于对照组 [分别为 :(9 1± 3 3)mmol/L与 (5 3± 0 7)mmol/L ;(15 8± 5 0 )mmol/L与 (8 5± 2 4 )mmol/L ;(2 96± 0 5 6 )与 (1 6 9± 0 82 )mmol/L及(15 3 80± 13 5 0 )ng/L与 (76 2 3± 10 78)ng/L ,均P <0 0 1],糖尿病组静息时的基础冠脉血流速度 (bFV)及TC、LDL C水平与对照组比较 ,差异均无显著性意义 (均P >0 0 5 ) ,而潘生丁注射后mFV及CFR (CFR =mFV/bFV)较对照组明显下降 [分别为 (5 8 1± 7 9)cm/s与 (73 5± 9 8)cm/s及 2 31± 0 4 9与 3 5 8± 0 4 6 ,P均 <0 0 1]。结论　老年糖尿病患者冠状动脉血流储备明显下降。     

胆固醇酯转运蛋白基因多态性在多囊卵巢综合征中的初步研究

目的:探讨胆固醇酯转运蛋白(CETP)在PCOS患者中的基因多态性和血脂、性激素的关系,以进一步认识PCOS脂代谢的特点。方法:应用PCR酶切方法检测108例PCOS患者及60例对照组的CETPTaqIB位点基因多态性。结果:CETPTaqIB基因频率及基因型分布在两组间分布差异无显著性。结论:CETPTaqIB基因多态性影响PCOS患者的HDLC水平,该基因在PCOS患者分布与正常人群分布无差异性。     

卵巢癌中蛋白激酶C的表达及其临床意义

目的　探讨上皮性卵巢癌组织蛋白激酶C (proteinkinaseC ,PKC)的表达和化疗耐药的关系 ,以及与P -糖蛋白 (P -gp)的相关性。方法　用免疫组化S -P法检测 35例卵巢上皮性肿瘤组织、 2 0例卵巢良性肿瘤组织和 2 0例正常卵巢组织中PKC和P -gp的表达 ,并进行相关临床因素分析。结果　①PKC、P -gp在卵巢恶性肿瘤中的表达明显高于在良性及正常组织中的表达 ;并且PKC和P -gp的表达有相关性 (P <0 0 5 ) ;②卵巢癌PKC的表达与临床病理因素无直接关系 ;③恶性肿瘤中 ,初治和复发的PKC表达阳性率分别为 34 8%和 75 % ;④化疗对PKC表达阳性和阴性卵巢癌患者的有效率分别为 2 3 5 %、 6 6 7% (P <0 0 5 ) ;⑤PKC表达阴性患者的预后优于阳性者 (P =0 0 39)。结论　PKC表达与卵巢癌组织化疗耐药明显相关 ,可能在P -gp介导的卵巢癌多药耐药中起重要作用。     

Laparoscopic splenectomy for isolated parenchymal splenic metastasis of ovarian cancer

Metastatic carcinoma of the spleen occurs in a setting of widespread malignant disease. Solitary parenchymal splenic metastasis of ovarian carcinoma is rare. We report a case of a 59-year-old woman who presented with an elevated serum CA125 level due to a solitary splenic metastasis after a long disease-free period. She was treated with laparoscopic splenectomy followed by chemotherapy. The literature contains 16 cases of solitary parenchymal splenic metastasis of ovarian carcinoma. Our case is the third case that was treated with laparoscopic splenectomy. We review the literature, and we focus on the laparoscopic approach in managing these cases.