Ovarian cancer is the fifth leading cause of cancer death among women in the U.S. and kills approximately 14,000 women each year (Nezhat et al., 2015). Survival increases with early diagnosis; the five-year survival rate in stage I is 90%. Symptoms are vague and common to many health diseases, which may well explain why upwards of 70% of women with ovarian cancer are diagnosed at stage III or IV (Slatnik & Duff, 2015). Preventative guidelines in the U.S. do not recommend screening for ovarian cancer in women of average risk (AAFP, 2016b; ACOG, 2011; Doubeni et al., 2016; Moyer, 2012; NCCN, 2015; Qaseem et al., 2014; Wilt et al., 2015). A lack of screening recommendations and a subtle presentation point to the need for greater healthcare professional recognition of symptoms and risk factors of ovarian cancer, which can then lead to a prompt diagnosis. While healthcare professionals have the opportunity to improve women’s health, gaps in knowledge exist related to ovarian cancer risk factors and symptom recognition (Gajjar et al., 2012). Continuing education improves healthcare professionals’ performance and patient health outcomes (Cervero & Gaines, 2015). Increasing healthcare professionals’ knowledge of ovarian cancer may help to detect ovarian cancer in earlier stages and enhance health outcomes of women. Based on the need for an increase in awareness and knowledge among healthcare professionals, a local ovarian cancer conference was developed and offered to healthcare professionals. The conference focused on presenting ovarian cancer risk factors and symptoms. Attendees were provided with an ovarian cancer resource for patient education. The conference was evaluated through pretests and posttests and a conference evaluation survey. Data was collected the evening of the conference with 29 attendees responding. After the conference, correct responses increased in the areas of risk factor and symptom recognition. The number of correct responses increased from 106 on the pretest to 122 on the posttest. In regards to ability to educate women about ovarian cancer, 62% of respondents indicated that they were “very confident” in their ability. / Pam Solseng Ovarian Cancer Endowment Fund

Call number: LD2668 .T4 1928 D61

No description available.

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

published_or_final_version / abstract / Obstetrics and Gynaecology / Master / Master of Philosophy

published_or_final_version / Pathology / Master / Master of Medical Sciences

published_or_final_version / Obstetrics and Gynaecology / Doctoral / Doctor of Philosophy

Ovarian carcinoma is the most lethal gynecological malignancy. The high relapse and mortality rates are attributable to late diagnosis and development of drug resistance. Identifying novel prognostic and therapeutic targets for ovarian carcinoma is crucial for improving patients' long-term survival rate. Forkhead box protein M1 (FOXM1), which is a widely studied member of the FOX superfamily of proteins, participates in cell proliferation and apoptosis affecting the developmental function of many organs. Recently, there has been emerging evidence supporting the biological significance of FOXM1 in carcinogenesis. Overexpression of FOXM1 has been reported in multiple human malignancies including primary breast cancer, lung cancer, prostate cancer, etc. However, whether FOXM1 participates in the development of ovarian cancer, with emphasis on the association with clinicopathological parameters and chemoresistance, remains unknown. This study aims at elucidating the functional role of FOXM1 in the tumorigenesis of ovarian cancer. Immunohistochemical study showed higher nuclear FOXM1 expression was significantly associated with advanced stages of ovarian cancer (P=0.035). Though not reaching statistical significance, FOXM1 overexpression displayed association with serous histologic subtype, high grade cancers (poor differentiation) and chemoresistance. Patients with a low FOXM1 level had a significantly longer overall (P=0.019) and disease-free survival (P=0.014) than those with high FOXM1 expression. Multivariate progression analysis established high expression of FOXM1, advanced cancer stages and poor histological differentiation (high grade) as independent prognostic factors for short overall and disease-free survival. Consistently, in vitro Transwell assays demonstrated transient knockdown of FOXM1 was capable of reducing SKOV-3 migration and invasion. Furthermore, paclitaxel treatment down-regulated FOXM1 expression in the sensitive cell line but not the resistant one. Immunofluorescence and flow cytometric analyses demonstrated FOXM1 knockdown could enhance paclitaxel-mediated mitotic catastrophe in ovarian cancer cells. Recent attention has been drawn to the oncogenic roles of kinesin-like protein KIF2C and p21-activated kinase 4 (PAK4) in human cancers. Interestingly, the expressions of KIF2C and PAK4 altered in a similar pattern to FOXM1 expression upon paclitaxel treatment by displaying down-regulation only in the paclitaxel sensitive cell line but not the resistant one. FOXM1 silencing, qPCR, luciferase reporter assay and chromatin immunoprecipitation confirmed KIF2C and PAK4 to be novel transcriptional targets of FOXM1. Clonogenic assay showed KIF2C knockdown could re-sensitize resistant cell line to paclitaxel treatment. Flow cytometry demonstrated KIF2C silencing was able to increase the number of cells blocked at G2/M cell cycle phase in sensitive cell line and raise the number of apoptotic cells in resistant cell line. Up-regulations of miR-590 and miR-370 were also observed in a panel of drug resistant ovarian and breast cancer cell lines. While ectopic expression of miR-590 reduced FOXM1 expression, FOXM1 also seemed to be able to regulate the expression of miR-590. In summary, this study showed overexpression of FOXM1 in ovarian cancer correlated with poor survival of patients and paclitaxel resistance. KIF2C and PAK4 were identified as novel transcriptional targets of FOXM1 implicated in chemoresistance. / published_or_final_version / Pathology / Doctoral / Doctor of Philosophy

by Chung Chi Kong, Arthur. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1992. / Includes bibliographical references (leaves 154-175). / Abstract --- p.i / Acknowledgements --- p.iv / Table of contents --- p.v / List of tables --- p.x / Chapter Chapter 1 --- General introduction --- p.1 / Chapter Chapter 2 --- Literature Review / Chapter 2.1 --- Ovarian maturation of decapod crustaceans / Chapter 2.1.1 --- Female reproductive system --- p.5 / Chapter 2.1.2 --- Ovarian maturation --- p.7 / Chapter 2.1.2.1 --- Previtellogenic stage --- p.11 / Chapter 2.1.2.2 --- Vitellogenic stage --- p.12 / Chapter 2.2 --- Factors affecting ovarian maturation in decapod crustaceans / Chapter 2.2.1 --- Endocrine control --- p.16 / Chapter 2.2.1.1 --- Inhibitory control --- p.17 / Chapter 2.2.1.2 --- Stimulatory control / Chapter 2.2.1.2.1 --- Gonad stimulating hormone (GSH) --- p.18 / Chapter 2.2.1.2.2 --- Vitellogenin stimulating ovarian hormone (VSOH) --- p.19 / Chapter 2.2.1.2.3 --- Ecdysteriods (MH) --- p.20 / Chapter 2.2.1.2.4 --- Juvenoids (JH) --- p.21 / Chapter 2.2.1.2.5 --- Pheromones --- p.22 / Chapter 2.2.1.2.6 --- Vertebrate-like steroids --- p.22 / Chapter 2.2.2 --- Environmental factors --- p.23 / Chapter 2.2.3 --- Nutritional factors --- p.26 / Chapter 2.3 --- The role of lipids during ovarian maturation of decapod crustaceans / Chapter 2.3.1 --- Lipids in decapod crustaceans --- p.29 / Chapter 2.3.2 --- Variation of lipids during ovarian maturation / Chapter 2.3.2.1 --- Introduction --- p.33 / Chapter 2.3.2.2 --- Changes of lipids in the ovary --- p.36 / Chapter 2.3.2.3 --- Changes of lipids in the hepatopancreas --- p.41 / Chapter Chapter 3 --- Variation of lipid composition during ovarian maturation of Penaeus chinensis / Chapter 3.1 --- Introduction --- p.46 / Chapter 3.2 --- Materials and methods / Chapter 3.2.1 --- Experimental animals --- p.46 / Chapter 3.2.2 --- Total lipid extraction and quantification --- p.47 / Chapter 3.2.2.1 --- Total lipid extraction --- p.48 / Chapter 3.2.2.2 --- Quantification of total lipid content --- p.48 / Chapter 3.2.3 --- Separation and quantification of lipid classes --- p.49 / Chapter 3.2.3.1 --- Separation of total lipid classes --- p.49 / Chapter 3.2.3.2 --- Separation of polar lipid classes --- p.50 / Chapter 3.2.3.3 --- Quantification of lipid classes --- p.51 / Chapter 3.2.4 --- Fatty acid analysis / Chapter 3.2.4.1 --- Preparation of fatty acid methyl ester (FAME) --- p.52 / Chapter 3.2.4.2 --- Gas chromatography --- p.53 / Chapter 3.3 --- Results / Chapter 3.3.1 --- Biometric data --- p.54 / Chapter 3.3.2 --- Variation of total lipids --- p.54 / Chapter 3.3.3 --- Variation of lipids in ovary / Chapter 3.3.3.1 --- Neutral lipid classes --- p.55 / Chapter 3.3.3.2 --- Polar lipid classes --- p.56 / Chapter 3.3.3.3 --- Fatty acid composition --- p.56 / Chapter 3.3.4 --- Variation of lipids in hepatopancreas / Chapter 3.3.4.1 --- Neutral lipid classes --- p.57 / Chapter 3.3.4.2 --- Polar lipid classes --- p.58 / Chapter 3.3.4.3 --- Fatty acid composition --- p.58 / Chapter 3.3.5 --- Variation of lipids in muscle / Chapter 3.3.5.1 --- Neutral lipid classes --- p.59 / Chapter 3.3.5.2 --- Polar lipid classes --- p.60 / Chapter 3.3.5.3 --- Fatty acid composition --- p.60 / Chapter 3.4 --- Discussion / Chapter 3.4.1 --- Variation of lipids in ovary during ovarian maturation --- p.88 / Chapter 3.4.2 --- Variation of lipids in hepatopancreas during ovarian maturation --- p.92 / Chapter 3.4.3 --- Variation of lipids in muscle during ovarian maturation --- p.95 / Chapter 3.4.4 --- Mobilization of lipids during ovarian maturation --- p.96 / Chapter Chapter 4 --- Variation of lipid composition during ovarian maturation of Metapenaeus ensis / Chapter 4.1 --- Introduction --- p.101 / Chapter 4.2 --- Materials and methods / Chapter 4.2.1 --- Experimental animals --- p.101 / Chapter 4.2.2 --- Total lipid extraction and quantification --- p.102 / Chapter 4.2.3 --- Separation and quantification of lipid classes --- p.102 / Chapter 4.2.4 --- Fatty acid analysis --- p.103 / Chapter 4.3 --- Results / Chapter 4.3.1 --- Biometric data --- p.104 / Chapter 4.3.2 --- Variation of total lipids --- p.104 / Chapter 4.3.3 --- Variation of lipids in ovary / Chapter 4.3.3.1 --- Neutral lipid classes --- p.105 / Chapter 4.3.3.2 --- Polar lipid classes --- p.105 / Chapter 4.3.3.3 --- Fatty acid composition --- p.106 / Chapter 4.3.4 --- Variation of lipids in hepatopancreas / Chapter 4.3.4.1 --- Neutral lipid classes --- p.107 / Chapter 4.3.4.2 --- Polar lipid classes --- p.108 / Chapter 4.3.4.3 --- Fatty acid composition --- p.109 / Chapter 4.3.5 --- Variation of lipids in muscle / Chapter 4.3.5.1 --- Neutral lipid classes --- p.109 / Chapter 4.3.5.2 --- Polar lipid classes --- p.109 / Chapter 4.3.5.3 --- Fatty acid composition --- p.110 / Chapter 4.4 --- Discussion / Chapter 4.4.1 --- Variation of lipids in ovary during ovarian maturation --- p.138 / Chapter 4.4.2 --- Variation of lipids in hepatopancreas during ovarian maturation --- p.142 / Chapter 4.4.3 --- Variation of lipids in muscle during ovarian maturation --- p.145 / Chapter 4.4.4 --- Mobilization of lipids during ovarian maturation --- p.146 / Chapter Chapter 5 --- General conclusions --- p.151 / References --- p.154

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