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Epithelial Ovarian Carcinoma (epithelial + ovarian_carcinoma)
Selected AbstractsLectin-based electrophoretic analysis of the expression of the 35,kDa inter-,-trypsin inhibitor heavy chain H4 fragment in sera of patients with five different malignanciesELECTROPHORESIS, Issue 12 2008Emida Mohamed Abstract A 35,kDa glycoprotein whose abundance was previously demonstrated to be enhanced in sera of patients with endometrial adenocarcinoma (n,=,12), was isolated from pooled sera of three of the cancer patients using champedak galactose-binding lectin affinity chromatography in the present study. Subjecting it to 2-DE and MS/MS, the glycoprotein was identified as the O -glycosylated fragment of inter-,-trypsin inhibitor heavy chain H4 (ITIH4). When compared to control sera (n,=,17), expression of the 35,kDa ITIH4 cleavage fragment was demonstrated to be significantly enhanced in sera of patients with breast carcinoma (n,=,10), epithelial ovarian carcinoma (n,=,10), and germ cell ovarian carcinoma (n,=,10) but not in patients with nasopharyngeal carcinoma (n,=,13) and osteosarcoma (n,=,7). The lectin-based electrophoretic bioanalytical method adopted in the present study may be used to assess the physiological relevance of ITIH4 fragmentation and its correlation with different malignancies, their stages and progression. [source] Expression of leukaemia inhibitory factor in epithelial ovarian carcinoma: correlation with clinical characteristicsHISTOPATHOLOGY, Issue 2 2008First page of article [source] Debulking surgery for incompletely operated advanced epithelial ovarian carcinomaJOURNAL OF SURGICAL ONCOLOGY, Issue 3 2009Murat Gultekin MD Abstract Background and Objectives There is still no any data about the role of re-operation and re-debulking in previously incompletely operated advanced staged patients with epithelial ovarian carcinoma (EOC). In this study, the authors aimed to analyze the effect of an incomplete primary surgery on patient prognosis. Methods Clinicopathological variables of 317 advanced staged EOC patients were retrospectively collected. Results Twenty-nine patients had an initial incomplete surgery and referred to our center for debulking while remaining 288 had undergone primary debulking surgery at our institution. Comparison of the two groups with respect to clinicopathological variables could not reveal significant difference. Median survival was 3.24 years for re-operated patients while it was 2.07 years for patients who had undergone primary debulking surgery. Upon multivariate analysis, final optimal debulking, tumor grade and a history of an incomplete surgery before the final debulking were the significant prognosticators. A subgroup analysis of re-staged patients could not reveal a significant role for either the type or the time interval between the operations. Conclusion A history of an incomplete primary surgery does not seem to adversely affect patient prognosis and the optimal cytoreductive success achieved in final debulking surgery is still the most important prognostic factor. J. Surg. Oncol. 2009;100:258,260. © 2009 Wiley-Liss, Inc. [source] Wilms tumor gene protein 1 is associated with ovarian cancer metastasis and modulates cell invasionCANCER, Issue 7 2008Maria V. Barbolina PhD Abstract BACKGROUND Although metastatic disease is the primary cause of death from epithelial ovarian carcinoma, to the authors' knowledge the cellular mechanisms that regulate intraperitoneal metastasis are largely unknown. Metastasizing ovarian carcinoma cells encounter a collagen-rich microenvironment because the submesothelial matrix is comprised mainly of interstitial collagens Types I and III. METHODS Immunohistochemistry using primary and metastatic ovarian carcinoma samples was employed to detect expression of Wilms tumor gene protein 1 (WT1). Three-dimensional (3D) collagen culture, real-time reverse transcriptase-polymerase chain reaction, and immunofluorescent staining were used to evaluate changes in WT1 RNA and protein expression in response to 3D collagen culture. Boyden chamber invasion assay, scratch-wound motility assay, and Western blot analysis were used to establish the function of WT1 in ovarian carcinoma cells. RESULTS To model intraperitoneal invasion in vitro, ovarian cancer cells were cultured in a 3D collagen microenvironment. 3D collagen culture resulted in robust induction of WT1 at the mRNA and protein levels. WT1 expression was prevalent in primary ovarian tumors and was retained in paired peritoneal metastases. Functional studies supported a role for WT1 in intraperitoneal invasion, because siRNA knockdown of WT1 expression reduced the ability of ovarian cancer cells to invade 3D collagen gels. CONCLUSIONS The data from the current study identify a novel regulatory mechanism for the control of WT1 expression and provide evidence for a functional role of WT1 protein in the control of cellular invasive activity. Cancer 2008. ©2008 American Cancer Society. [source] Surgery by consultant gynecologic oncologists improves survival in patients with ovarian carcinomaCANCER, Issue 3 2006Mirjam J. A. Engelen M.D. Abstract BACKGROUND Consultant gynecologic oncologists from the regional Comprehensive Cancer Center assisted community gynecologists in the surgical treatment of patients with ovarian carcinoma when they were invited. For this report, the authors evaluated the effects of primary surgery by a gynecologic oncologist on treatment outcome. METHODS The hospital files from 680 patients with epithelial ovarian carcinoma who were diagnosed between 1994 and 1997 in the northern part of the Netherlands were abstracted. Treatment results were analyzed according to the operating physician's education by using survival curves and univariate and multivariate Cox regression analyses. RESULTS Primary surgery was performed on 184 patients by gynecologic oncologists, and on 328 patients by general gynecologists. Gynecologic oncologists followed surgical guidelines more strictly compared with general gynecologists (patients with International Federation of Gynecology and Obstetrics [FIGO] Stage I,II disease, 55% vs. 33% [P = 0.01]; patients with FIGO Stage III disease, 60% vs. 40% [P = 0.003]) and more often removed all macroscopic tumor in patients with FIGO Stage III disease (24% vs. 12%; P = 0.02). When patients were stratified according to FIGO stage, the 5-year overall survival rate was 86% versus 70% (P = 0.03) for patients with Stage I,II disease and 21% versus 13% (P = 0.02) for patients with Stage III,IV disease who underwent surgery by gynecologic oncologists and general gynecologists, respectively. The hazards ratio for patients who underwent surgery by gynecologic oncologists was 0.79 (95% confidence interval [95%CI], 0.61,1.03; adjusted for patient age, disease stage, type of hospital, and chemotherapy); when patients age 75 years and older were excluded, the hazards ratio fell to 0.71 (95% CI, 0.54,0.94) in multivariate analysis. CONCLUSIONS The surgical treatment of patients with ovarian carcinoma by gynecologic oncologists occurred more often according to surgical guidelines, tumor removal more often was complete, and survival was improved. Cancer 2006. © 2005 American Cancer Society. [source] Human epithelial ovarian carcinoma cell-derived cytokines cooperatively induce activated CD4+CD25,CD45RA+ naïve T cells to express forkhead box protein 3 and exhibit suppressive ability in vitroCANCER SCIENCE, Issue 11 2009Xiaofeng Zhao Regulatory T cells play an important role in tumor escape from host antitumor immunity. Increased frequencies of CD4+CD25+ regulatory T cells have been documented in the tumor sites, malignant effusions, and peripheral blood of patients with ovarian carcinoma. However, the mechanism involved remains unclear. In the present study, we collected high-purity human CD4+CD25,CD45RA+ naïve T cells by microbead cell separation. These cells did not express FOXP3 by single-cell analysis, and few cells expressed FOXP3 when they were activated with anti-CD3/CD28 dual signal. However, more cells expressed FOXP3 when the supernatant of human epithelial ovarian carcinoma cell culture was added, yet not the supernatant of normal human ovarian surface epithelia cell culture. Neutralization assays revealed that neutralizing antibody against transforming growth factor , (TGF-,), interleukin-10, and interleukin-4 did not abrogate elevated FOXP3 expression induced by carcinoma cell culture supernatant, whereas neutralizing leukemia inhibitory factor (LIF) partially abrogated FOXP3 expression, but LIF alone could not increase FOXP3 expression in activated naïve T cells. Further, an in vitro coculture suppression assay showed that these cells could suppress the proliferation of autologous CD4+CD25,CD45RA, T cells. In summary, our findings show that ovarian carcinoma cells are able to induce expression of FOXP3 and exhibit suppressive ability in activated naïve T cells by producing soluble substances, and multiple cytokines involve in the induction of FOXP3 expression. (Cancer Sci 2009) [source] Expression profiling correlates with treatment response in women with advanced serous epithelial ovarian cancerINTERNATIONAL JOURNAL OF CANCER, Issue 4 2006Tanya R. Newton Abstract The majority of epithelial ovarian carcinomas are of serous subtype, with most women presenting at an advanced stage. Approximately 70% respond to initial chemotherapy but eventually relapse. We aimed to find markers of treatment response that might be suitable for routine use, using the gene expression profile of tumor tissue. Thirty one women with histologically-confirmed late-stage serous ovarian cancer were classified into 3 groups based on response to treatment (nonresponders, responders with relapse less than 12 months and responders with no relapse within 12 months). Gene expression profiles of these specimens were analyzed with respect to treatment response and survival (minimum 36 months follow-up). Patients' clinical features did not correlate with prognosis, or with specific gene expression patterns of their tumors. However women who did not respond to treatment could be distinguished from those who responded with no relapse within 12 months based on 34 gene transcripts (p < 0.02). Poor prognosis was associated with high expression of inhibitor of differentiation-2 (ID2) (p = 0.001). High expression of decorin (DCN) and ID2 together was strongly associated with reduced survival (p = 0.003), with an estimated 7-fold increased risk of dying (95% CI 1.9,29.6; 14 months survival) compared with low expression (44 months). Immunohistochemical analysis revealed both nuclear and cytoplasmic distribution of ID2 in ovarian tumors. High percentage of nuclear staining was associated with poor survival, although not statistically significantly. In conclusion, elevated expression of ID2 and DCN was significantly associated with poor prognosis in a homogeneous group of ovarian cancer patients for whom survival could not be predicted from clinical factors. © 2006 Wiley-Liss, Inc. [source] Expression of heat-shock proteins hsp27, hsp70 and hsp90 in malignant epithelial tumour of the ovariesAPMIS, Issue 4 2003Correlation with clinicopathologic factors, survival Recently, considerable attention has been focused on the role of the small heat-shock protein group hsp27, hsp70 and hsp90 in the clinical outcome of several malignancies. However, conflicting data exist regarding the prognostic role of hsp27 expression in ovarian carcinoma, and the prognostic significance of hsp70 and hsp90 expression still remains unknown in these tumours. The purpose of this study was to investigate immunohistochemically whether hsp27, hsp70 and hsp90 expression was associated with clinicopathological parameters and survival in 52 epithelial ovarian carcinomas. Chi-square test, Kaplan-Meier and Cox regression analysis were used for statistical analysis. Among clinicopathological parameters, hsp27, hsp70 and hsp90 expression was only correlated with FIGO stage; hsp70 and hsp90 positivity failed to detect survival. However, the overall survival rate of patients with hsp27 expression was 13%, which was significantly worse than that of patients without hsp27 expression (47%) (p<0.01). The prognosis was also adversely affected by FIGO stage (p<0.01) and presence of ascites (p<0.01). In multivariate analysis, hsp27 expression and FIGO stage were independent prognostic variables. Our results indicate that hsp70 and hsp90 expression had no prognostic relevance in epithelial ovarian carcinomas. However, hsp27 expression and FIGO stage in these tumours could be reliable indicators of prognosis. [source] HuR expression in the nucleus correlates with high histological grade and poor disease-free survival in ovarian cancerAUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 1 2009Xiaofang YI Background: HuR, a nucleo-cytoplasmic shuttling protein, plays an important role in mRNA stability as well as cellular differentiation. Recently, HuR expression, particularly in the cytoplasm, was thought to be associated with the prognosis of several cancers including ovarian cancer. Aims: To study the clinical significance of nuclear HuR expression in ovarian cancer. Methods: Primary epithelial ovarian carcinomas (102) and ovarian low malignant potential tumours (11) were assessed for HuR protein expression by immunohistochemistry. HuR scoring accounted for both intensity and percentage of cells stained, and ranged from 0 to 300. Results: HuR was found to be present predominantly in the nucleus, where it was expressed in 85.8% of cases. Nuclear HuR was associated with the invasive cancers (P = 0.004), high grade (P < 0.0001), large residual disease (P = 0.045) and poor disease-free survival (P = 0.0009). Among those 91 specimens with high grade, 76.9% had a high nuclear HuR score, while in those 22 cases with low grade, only 31.8% had a high HuR score (P < 0.0001). Multivariate analysis showed that nuclear HuR intensity was an independent prognostic factor for poor disease-free survival (P = 0.0484). When the invasive cancers were analysed separately, only the association between nuclear HuR and high grade remained (P = 0.0089). Conclusions: Our results support the clinical significance of nuclear HuR in ovarian carcinoma and suggest that nuclear HuR may also play a role in the biology of ovarian cancer. These data suggest a more complex model for HuR in ovarian cancer than one limited to cytoplasmic localisation. [source] A review of p53 expression and mutation in human benign, low malignant potential, and invasive epithelial ovarian tumorsCANCER, Issue 2 2003Leanne M. Kmet M.Sc. Abstract BACKGROUND In the current study, the authors present pooled data from studies that investigated p53 protein expression and/or mutation in human epithelial ovarian tumors. METHODS The English literature in the MEDLINE, PubMed, and Ingenta databases was searched to the end of the year 2000 to identify relevant studies. Data were pooled across eligible studies, and the prevalence of p53 expression and mutation among benign, low malignant potential (LMP), and invasive tumors was determined. Prevalence estimates by tumor histology, International Federation of Gynecology and Obstetrics (FIGO) stage, and grade also were calculated. RESULTS The pooled prevalence estimate for p53 overexpression among epithelial ovarian carcinomas was 51% (95% confidence intervals [95% CI], 50,53%) compared with 17% (95% CI, 15,20%) among LMP tumors and 7% (95% CI, 5,10%) among benign tumors. p53 mutation prevalence estimates were 45% (95% CI, 42,47%), 5% (95% CI, 2,9%), and 1% (95% CI, 0,5%), respectively, for invasive, LMP, and benign tumors. The prevalence of these p53 abnormalities was found to be associated positively with increasing tumor grade and stage. Differences based on histologic subtype also were found. CONCLUSIONS Although these pooled estimates might appear to offer support for various hypotheses regarding the role of p53 in ovarian carcinoma, the limitations inherent in these data hamper the interpretation of the significance of any of the findings. Future studies will require innovative methods to address the limitations of many previous investigations and more comprehensive investigation into defective tumor suppression mechanisms. Cancer 2003;97:389,404. © 2003 American Cancer Society. DOI 10.1002/cncr.11064 [source] | ||||||||||