OBJECTIVE: Much of the early investigative work on the usefulness of preoperative serum CA-125 levels in identifying patients with early-stage endometrial carcinoma who have occult metastases were carried out in Europe and the United States. This article reviews CA-125 as a possible index for determining the need for full surgical staging, from the results of large medical centers in Asia, particularly Taiwan and Korea. METHODS: A Medline search was performed using CA-125 and endometrial cancer as index words from 1981 to 2012. Those publications felt to be the most important especially from institutions from Asia since 2000 were identified in this review. RESULTS: Most articles that analyzed the utility of serum CA-125 levels as predictive marker for disease extent or prognosis in uterine cancer used univariate and multivariable logistic regression analysis, and performed receiver operative curves to find the best cut-off values. The main factor of interest was whether clinicians can stratify patients that need lymphadenectomy in early stage disease. Suggested optimal cut-off value ranged from 20 to 210 U/mL. Not only preoperative CA-125 level, but myometrial invasion status by magnetic resonance imaging was the most significant combined parameter for predicting disease extent. CONCLUSION: Elevated CA-125 in patients with apparent early-stage disease is clearly a risk factor for the presence of extra-uterine disease although the optimal cut-off levels vary. The evolution of clinical investigations over the past decade, particularly in Asia, suggests employment of the test in a more focused manner to identify high risk patients preoperatively.
Asia ; Asian Continental Ancestry Group ; CA-125 Antigen ; Employment ; Endometrial Neoplasms ; Europe ; Female ; Humans ; Logistic Models ; Lymph Node Excision ; Magnetic Resonance Imaging ; Neoplasm Metastasis ; Neoplasm Staging ; Prognosis ; Risk Factors ; Taiwan ; United States ; Uterine Neoplasms

No abstract available.

No abstract available.
Female ; Granulosa Cell Tumor ; Granulosa Cells

Fetal chylothorax is a rare congenital manifestation that shows variable clinical outcome ranging from complete spontaneous resolution to progression into hydrops or lung hypoplasia. There is no consensus in the literature as to the optimal antenatal management despite several complications such as preterm delivery, pulmonary hypoplasia, and perinatal death. Pleuroamniotic shunting has been the treatment of choice in fetal chylothorax. Recently, new fetal therapy such as OK-432 (Picibanil) pleurodesis is being introduced. Herein, we present two cases of women referred at early 2nd trimester because of fetal hydrothorax by routine ultrasonography. Cytology obtained by thoracocentesis revealed abundant lymphocytes, suggesting chylothorax. Effusion was aspirated and OK-432 (Picibanil) was injected into the pleural space of fetus. On follow up ultrasonography, the pleural effusion was nearly resolved by adhesion of the intrathoracic space and resulted in the delivery of a healthy neonate. Intrapleural OK-432 injection may be feasible therapeutic option for selected cases in early 2nd trimester with persistent chylothorax for effective control of pleural effusion with no adverse effects.
Chylothorax ; Consensus ; Edema ; Female ; Fetal Therapies ; Fetus ; Follow-Up Studies ; Humans ; Hydrothorax ; Infant, Newborn ; Lung ; Lymphocytes ; Picibanil ; Pleural Effusion ; Pleurodesis

PURPOSE: The aim of this study was to compare survival of patients with uterine sarcomas using the 1988 and 2008 International Federation of Gynecologists and Obstetricians (FIGO) staging systems to determine if revised 2008 staging accurately predicts patient survival. MATERIALS AND METHODS: A total of 83 patients with leiomyosarcoma and endometrial stromal sarcoma treated at Yonsei University Health System between March of 1989 and November of 2009 were reviewed. The prognostic validity of both FIGO staging systems, as well as other factors was analyzed. RESULTS: Leiomyosarcoma and endometrial stromal sarcoma comprised 47.0% and 53.0% of this study population, respectively. Using the new staging system, 43 (67.2%) of 64 eligible patients were reclassified. Among those 64 patients, 45 (70.3%) patients with limited uterine corpus involvement were divided into stage IA (n=14) and IB (n=31). Univariate analysis demonstrated a significant difference between stages I and II and the other stages in both staging systems (p<0.001) with respect to progression-free survival and overall survival (OS). Age, menopausal status, tumor size, and cell type were significantly associated with OS (p=0.011, p=0.031, p=0.044, p=0.009, respectively). In multivariate analysis, revised FIGO stage greater than III was an independent poor prognostic factor with a hazard ratio of 9.06 [95% confidence interval (CI) 2.49-33.0, p=0.001]. CONCLUSION: The 2008 FIGO staging system is more valid than the previous FIGO staging system for uterine sarcomas with respect to its ability to distinguish early-stage patients from advanced-stage patients.
Adult ; Disease-Free Survival ; Female ; Humans ; Leiomyosarcoma/mortality/pathology ; Male ; Middle Aged ; Neoplasm Staging ; Prognosis ; Uterine Neoplasms/*mortality/*pathology

Extra-ovarian yolk sac tumor arising in the omentum is extremely rare. As yolk sac tumor originated from the omentum has been rarely reported, its clinical information is very limited. The authors encountered a case of yolk sac tumor originated from the omentum, and reported the case herein. A 32-year-old woman was presented with developed low abdominal distension for a month. Magnetic resonance imaging findings were suggestive of ovarian malignancy with ascites and peritoneal seeding nodules. Explorative laparotomy was performed and then the findings from frozen biopsy of omentum were suggestive of poorly differentiated tumor though whether it was primary or metastatic was uncertain. Thus, staging laparotomy were performed. Histopathology confirmed that the tumor was a yolk sac tumor of omentum origin. Then, 6 cycles of postoperative adjuvant chemotherapy at intervals of 3 weeks were performed using bleomycin, etoposide, and cisplatin regimen. Four-year outpatient follow-up thereafter showed no relapse.
Adult ; Ascites ; Biopsy ; Bleomycin ; Chemotherapy, Adjuvant ; Cisplatin ; Endodermal Sinus Tumor* ; Etoposide ; Female ; Follow-Up Studies ; Humans ; Laparotomy ; Magnetic Resonance Imaging ; Omentum* ; Outpatients ; Rare Diseases ; Yolk Sac

PURPOSE: Celecoxib, a highly selective cyclooxygenase-2 inhibitor, regulates apoptosis of several types of human cancer cells. The purpose of this study was to investigate whether celecoxib in combination with paclitaxel modulates apoptosis of ovarian cancer cells, and to identify the signal pathway by which celecoxib mediates apoptosis. MATERIALS AND METHODS: OVCAR-3 cells were exposed to paclitaxel (20 microM) in the absence or presence of celecoxib (10 microM). Cell viability was evaluated using a Cell Counting Kit-8 assay. Apoptosis was evaluated using Annexin-V/7-aminoactinomycin D staining and a cellular DNA fragmentation enzyme-linked immunosorbent assay. Caspase-3, -9, and cleavage of poly ADP-ribose polymerase (PARP) were determined by western blotting. Expression of nuclear factor-kappaB (NF-kappaB) and vascular endothelial growth factor (VEGF) and Akt activation were assessed using reverse transcriptase-polymerase chain reaction and western blotting. RESULTS: Celecoxib enhanced paclitaxel-induced growth inhibition of OVCAR-3 cells. Celecoxib significantly increased paclitaxel-induced apoptosis of OVCAR-3 cells. Pretreatment with celecoxib also increased activation of caspase-9, -3 and cleaved PARP following paclitaxel-treatment. Exposure of OVCAR-3 cells to celecoxib in combination with paclitaxel resulted in downregulation of NF-kappaB activation and VEGF expression. Furthermore, combining celecoxib and paclitaxel inhibited phosphorylation of Akt. CONCLUSION: OVCAR-3 cells were sensitized to paclitaxel-induced apoptosis by celecoxib through downregulation of NF-kappaB and Akt activation, suggesting that celecoxib may work synergistically with paclitaxel to inhibit different targets and ultimately produce anticancer effects. Combining celecoxib with paclitaxel may prove beneficial in the clinical treatment of ovarian cancer.
Adenosine Diphosphate Ribose ; Apoptosis* ; Blotting, Western ; Caspase 3 ; Caspase 9 ; Cell Count ; Cell Line* ; Cell Survival ; Cyclooxygenase 2 ; DNA Fragmentation ; Down-Regulation ; Enzyme-Linked Immunosorbent Assay ; Humans* ; NF-kappa B ; Ovarian Neoplasms* ; Paclitaxel ; Phosphorylation ; Signal Transduction ; Vascular Endothelial Growth Factor A ; Celecoxib

PURPOSE: Celecoxib, a highly selective cyclooxygenase-2 inhibitor, regulates apoptosis of several types of human cancer cells. The purpose of this study was to investigate whether celecoxib in combination with paclitaxel modulates apoptosis of ovarian cancer cells, and to identify the signal pathway by which celecoxib mediates apoptosis. MATERIALS AND METHODS: OVCAR-3 cells were exposed to paclitaxel (20 microM) in the absence or presence of celecoxib (10 microM). Cell viability was evaluated using a Cell Counting Kit-8 assay. Apoptosis was evaluated using Annexin-V/7-aminoactinomycin D staining and a cellular DNA fragmentation enzyme-linked immunosorbent assay. Caspase-3, -9, and cleavage of poly ADP-ribose polymerase (PARP) were determined by western blotting. Expression of nuclear factor-kappaB (NF-kappaB) and vascular endothelial growth factor (VEGF) and Akt activation were assessed using reverse transcriptase-polymerase chain reaction and western blotting. RESULTS: Celecoxib enhanced paclitaxel-induced growth inhibition of OVCAR-3 cells. Celecoxib significantly increased paclitaxel-induced apoptosis of OVCAR-3 cells. Pretreatment with celecoxib also increased activation of caspase-9, -3 and cleaved PARP following paclitaxel-treatment. Exposure of OVCAR-3 cells to celecoxib in combination with paclitaxel resulted in downregulation of NF-kappaB activation and VEGF expression. Furthermore, combining celecoxib and paclitaxel inhibited phosphorylation of Akt. CONCLUSION: OVCAR-3 cells were sensitized to paclitaxel-induced apoptosis by celecoxib through downregulation of NF-kappaB and Akt activation, suggesting that celecoxib may work synergistically with paclitaxel to inhibit different targets and ultimately produce anticancer effects. Combining celecoxib with paclitaxel may prove beneficial in the clinical treatment of ovarian cancer.
Adenosine Diphosphate Ribose ; Apoptosis* ; Blotting, Western ; Caspase 3 ; Caspase 9 ; Cell Count ; Cell Line* ; Cell Survival ; Cyclooxygenase 2 ; DNA Fragmentation ; Down-Regulation ; Enzyme-Linked Immunosorbent Assay ; Humans* ; NF-kappa B ; Ovarian Neoplasms* ; Paclitaxel ; Phosphorylation ; Signal Transduction ; Vascular Endothelial Growth Factor A ; Celecoxib

PURPOSE: The biological function of long non-coding RNAs (lncRNAs) is only partially understood; therefore, in this study, we investigated the expression of the novel HOXA11 antisense (HOXA11as) lncRNA and its oncogenic role in serous ovarian cancer (SOC). MATERIALS AND METHODS: HOXA11as expression was examined in 129 SOC tissue samples by real time reverse transcription polymerase chain reaction. Clinicopathological factors and patient survival were compared between the high (n=27) and low HOXA11as expression group (n=102). To investigate the role of HOXA11as in cell proliferation, invasion, and migration, HOXA11as expression in ovarian cancer cells was knocked down using RNA interference. RESULTS: HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue (p < 0.05). Higher HOXA11as expression was significantly correlated with histological grade (p=0.017) and preoperative cancer antigen 125 (p=0.048). HOXA11as overexpression in SOC cells led to increased cell proliferation, invasion, and migration. Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including vascular endothelial growth factor, matrix metalloproteinase 9 (MMP-9), B-catenin, E-cadherin, Snail, Twist, and vimentin. Multivariate analysis revealed that HOXA11as was a prognostic factor of progressive disease and mortality (hazard ratio [HR], 1.730; p=0.043 and HR, 2.170; p=0.033, respectively). Progression-free and overall survival were significantly shorter in patients with high HOXA11as expression. CONCLUSION: These findings highlight the clinical significance of HOXA11as to predicting the prognosis of SOC patients and suggest its potential in promoting tumor aggressiveness via regulation of vascular endothelial growth factor (VEGF), MMP-9, and EMT-related mechanisms.
Cadherins ; Cell Proliferation* ; Epithelial-Mesenchymal Transition ; Humans ; Matrix Metalloproteinase 9 ; Mortality ; Multivariate Analysis ; Ovarian Neoplasms* ; Polymerase Chain Reaction ; Prognosis* ; Reverse Transcription ; RNA Interference ; RNA, Long Noncoding* ; Snails ; Vascular Endothelial Growth Factor A ; Vimentin

The 34th Annual Meeting of Korean Society of Gynecologic Oncology (KSGO) was held in Busan, Korea from 26 to 27 April. Around 460 Korean and international clinicians gathered in Busan to share and discuss their latest work and key issues of gynecologic oncologic research and treatment. The scope of this meeting included recent clinical trials and updates in gynecologic oncology, advances in ovarian cancer treatment, targeted therapy and immunotherapy in gynecologic cancer, management of hereditary gynecologic cancer, and newly revised staging of cervical cancer. As expected, the ongoing debate regarding the recent clinical trial on minimally invasive surgery for early-stage cervical cancer was addressed throughout the congress and the initial outline of the KSGO position statement was open for discussion. The meeting was an opportunity for all participants to come together and explore scientific insights of gynecologic cancer.
Busan ; Endometrial Neoplasms ; Female ; Immunotherapy ; Korea ; Minimally Invasive Surgical Procedures ; Molecular Targeted Therapy ; Ovarian Neoplasms ; Uterine Cervical Neoplasms