Epithelial Ovarian Cancer: A Review of Current Management

Guppy, Amy; Nathan, Paul; Rustin, G. J. S.

doi:10.1016/j.clon.2005.05.009

Cited by 101 publications

(71 citation statements)

References 133 publications

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“…Our finding is closer to the observations made in several other studies i.e. 64%, 66% and 70% [7,24,25] respectively. However, Guppey et al [26] documented a higher incidence of epithelial tumours than in our study i.e.…”

Section: Discussionsupporting

confidence: 91%

"Ovarian Neoplasms- Histopathological Patterns and Relative Frequencies in an Indian Tertiary Care Hospital"

2017

IJCRR

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Introduction: Ovarian neoplasms are tumors or cancer of the ovary. These neoplasms can be benign or malignant and are classified according to the tissue of origin, such as the surface epithelium, the stromal endocrine cells, and the totipotent germ cells.Ovarian neoplasms are one of the major causes of gynaecological problems in females and present with marked variation in their histological types. Western and Asian countries show a difference in relative frequency of these lesions. This study was conducted to find out frequency of various histological patterns of ovarian neoplasms received as surgical pathology specimens at Histopathology department, Civil Hospital, Ahmedabad.

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Section: Discussionsupporting

confidence: 91%

"Ovarian Neoplasms- Histopathological Patterns and Relative Frequencies in an Indian Tertiary Care Hospital"

2017

IJCRR

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“…Survival in cases of ovarian cancer is low. Treatment consists of surgery, with the attempt to remove the entire tumor or to leave less than 1 cm of residual tumor followed by platinum-based chemotherapy (20) . Despite the fact that the residual disease is an important prognostic factor, some patients who underwent optimal cytoreduction acquired resistance to chemotherapy and experienced low rates of survival.…”

Section: Resultsmentioning

confidence: 99%

Assessment of glutathione S-transferaseM1 (GSTM1) and its polymorphisms GSTM1 null in the response to treatment with chemotherapy in advanced ovarian carcinoma

Takeda

Leite

Junqueira

et al. 2011

Einstein (São Paulo)

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Objective: To assess if the genotype of the glutathione S-transferase M1 (GSTM1) enzyme and its GSTM1 null polymorphism can influence the response to chemotherapeutic treatment of advanced ovarian cancer. Methods: Case-control study of 112 patients with advanced ovarian cancer submitted to chemotherapy during the period from January 1995 to December 2005. The tissue to study the GSTM1 genotype and its deletion came from surgical staging to treat ovarian cancer. The PCR product generates two distinct genotypes, characterized as positive and null. The response to chemotherapy was evaluated using the World Health Organization (WHO) criteria. Patients were classified as having: a) no response, b) a response. Results: The presence of GSTM1 or its GSTM1 null polymorphism did not influence the preoperative chemotherapy response. Among the patients who did respond, 88.9% presented with positive GSTM1 and 11.1% with null GSTM1. Among the patients that did not respond, 85.71% presented with positive GSTM1 and 14.29% with null GSTM1 (p = 0.825). GSTM1 and its GSTM1 null polymorphism had no influence on the postoperative response to chemotherapy. Among the patients who did respond, 80.65% presented with positive GSTM1 and 19.35% with null GSTM1. Among the patients who did not respond, 87.50% presented with positive GSTM1 and 12.5% with the null polymorphism (p = 0.553). Conclusion: No difference was observed in the response to treatment with chemotherapy in patients with advanced ovarian cancer, as to the GSTM1 genotype compared to its GSTM1 null polymorphism.

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“…The presence of MSI as a consequence of the ovulatory process reinforces the importance of certain clinical risk factors, including early menarche, late menopause and infertility, while factors that decrease the number of ovulatory cycles, such as pregnancy, lactation and contraceptive use, reduce the risk of ovarian cancer throughout life (25).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of microsatellite instability in women with epithelial ovarian cancer

et al. 2012

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Abstract. The function of microsatellite instability (MSI) and the optimal panel of markers for epithelial ovarian cancer (EOC) are not well established. This study aimed to use the National Cancer Institute (NCI) markers BAT25, BAT26, D2S123, D5S346 and D17S250 to evaluate MSI in patients with ovarian serous cystadenocarcinoma, compared with ovarian serous cystadenoma and normal ovaries. A total of 37 patients were divided into three groups, as follows: cystadenocarcinoma (n=13), cystadenoma (n=10) and normal ovaries (n=14). DNA was extracted with TRIzol and quantified by spectrophotometry. MSI was evaluated by polymerase chain reaction (PCR), and classified as high (MSI-H), low (MSI-L) or stable (MSS). FIGO staging was I/II in 23.1% and III/IV in 76.9% of the cystadenocarcinoma group. Polymorphisms were found using at least one marker in 32 women, and were observed with D2S123 (83.7%), D17S250 (81.1%), D5S346 (72.9%), BAT25 (21.6%) and BAT26 (16.2%) markers. In the cystadenocarcinoma group, BAT25, BAT26, D2S123, D5S346 and D17S250 markers were positive in 30.8, 76.9, 53.8, 69.2 and 69.2% of patients, respectively. The same markers were positive in 30, 50, 40, 60 and 30% of the cystadenoma group, and 50, 71.4, 71.4, 64.3 and 63.3% in the normal ovary group, respectively. MSI-H was present in 84.6, 60 and 78.6% of the cystadenocarcinoma, cystadenoma and normal patients, respectively. MSI-L was detected in 0, 30 and 7.1%, and MSS was identified in 15.4, 10 and 14.3% of the cystadenocarcinoma, cystadenoma and normal patients, respectively. The frequency of MSI in both benign epithelial ovarian neoplasms and in normal ovaries was high, as well as in EOC, with no statistically significant difference between the groups. This suggests that MSI may arise as a consequence of the ovulatory process, and not solely as a feature of malignant ovarian tumors. IntroductionEpithelial ovarian cancer (EOC) has a high mortality rate (1); it is the leading cause of death among gynecological tumors, and the fourth leading cause of cancer-related mortality among women in the United States (2). Due its nonspecific symptoms and lack of effective screening methods (3), approximately two-thirds of cases are diagnosed in stages III and IV, with a five-year survival rate of 10-20% (4,5). Approximately 90% of ovarian tumors originate from epithelial cells (6,7). The mortality rate has not changed in the last two decades (8).A group of enzymes known as the DNA mismatch repair (MMR) system is responsible for repairing mutations. Hereditary nonpolyposis colorectal cancer (HNPCC) is the third leading cause of hereditary ovarian cancer, and is caused by mutations in genes of the MMR system. One of the consequences of deficient MMR is microsatellite instability (9), which carries somatic mutations in tumor suppressor genes, oncogenes, apoptosis and detoxification genes, and is involved in both the initiation and progression of tumors (10).HNPCC has been studied using a panel of five National Cancer Institute (NCI) markers, which includes two mono...

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Epithelial Ovarian Cancer: A Review of Current Management

Cited by 101 publications

References 133 publications

"Ovarian Neoplasms- Histopathological Patterns and Relative Frequencies in an Indian Tertiary Care Hospital"

"Ovarian Neoplasms- Histopathological Patterns and Relative Frequencies in an Indian Tertiary Care Hospital"

Assessment of glutathione S-transferaseM1 (GSTM1) and its polymorphisms GSTM1 null in the response to treatment with chemotherapy in advanced ovarian carcinoma

Evaluation of microsatellite instability in women with epithelial ovarian cancer

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