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MeSH Review:

Ovarian Neoplasms

Yajnik, V., Shayesteh, L., Gayther, S.A., Partridge, E.E., Merajver, S.D., et al.

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Disease relevance of Ovarian Neoplasms

We show that the EMSY gene is amplified almost exclusively in sporadic breast cancer (13%) and higher-grade ovarian cancer (17%) [1].
Steroid hormones are key regulators of numerous physiological and developmental processes, including metastasis of breast and ovarian cancer [2].
To define the role of BRCA2 in sporadic breast and ovarian cancer, we screened the entire gene for mutations using a combination of techniques in 70 primary breast carcinomas and in 55 primary epithelial ovarian carcinomas [3].
CONCLUSIONS: As compared with intravenous cisplatin, intraperitoneal cisplatin significantly improves survival and has significantly fewer toxic effects in patients with stage III ovarian cancer and residual tumor masses of 2 cm or less [4].
Hypercalcemia and ectopic secretion of parathyroid hormone by an ovarian carcinoma with rearrangement of the gene for parathyroid hormone [5].

Psychiatry related information on Ovarian Neoplasms

EVIDENCE: Studies evaluating cancer risk, surveillance, and risk reduction in individuals genetically susceptible to breast and ovarian cancer were identified using MEDLINE (National Library of Medicine) and from bibliographies of articles thus identified [6].
BACKGROUND: It has been hypothesized that physical activity may reduce the risk of ovarian cancer by decreasing estrogen levels, reducing body fat, and reducing the frequency of ovulation [7].
The first comparative study on predicting post-test distress (conceptualised by intrusion and avoidance, measured with the Impact of Event Scale) after presymptomatic genetic testing for Huntington's disease (HD, n=25), cancer syndromes (familial adenomatous polyposis (FAP, n=23)), and hereditary breast and ovarian cancer (HBOC, n=10) is reported [8].
RESULTS: There was non-random geographical distribution of AD PSD but not of the comparison conditions (vascular dementia (VaD), motor neurone disease, prostatic or ovarian cancers) [9].
The use of CA-125 for clinical decision making in ovarian cancer requires further investigation to determine and validate a prognostic index with acceptable sensitivity and specificity, and to determine the clinical impact of treatment decisions made using such an index [10].

High impact information on Ovarian Neoplasms

The significant risk factor for development of ovarian cancer is advancing age, although there is clearly a genetic predisposition--often associated with the BRCA1 and BRCA2 genes--in at least 5% to 10% of all epithelial ovarian cancers [11].
Standard postoperative therapy for advanced-stage ovarian cancer includes platinum-based chemotherapy with the substitution of paclitaxel for cyclophosphamide occurring in the last decade [11].
Ovarian cancer, Part II [12].
These findings suggest that OPCML is an excellent candidate for the 11q25 ovarian cancer TSG [13].
DOCK4 mutations are present in a subset of human cancer cell lines; a recurrent missense mutant identified in human prostate and ovarian cancers encodes a protein that is defective in Rap1 activation [14].

Chemical compound and disease context of Ovarian Neoplasms

Treatment of ovarian cancer with intraperitoneal cisplatin [15].
Acute leukemia after alkylating-agent therapy of ovarian cancer [16].
CONCLUSIONS: Platinum-based treatment of ovarian cancer increases the risk of secondary leukemia [17].
In a randomized, double-blind, placebo-controlled study, we assessed the efficacy of an ACTH(4-9) analogue, Org 2766, in the prevention of cisplatin neuropathy in 55 women with ovarian cancer [18].
Verapamil, a calcium channel blocking agent, completely reversed adriamycin resistance in human ovarian cancer cells with moderate (three- to sixfold) degrees of resistance and partially reversed resistance in highly (150-fold) resistant cells [19].

Biological context of Ovarian Neoplasms

We have analysed 60 families with a history of breast and/or ovarian cancer for germline mutations in BRCA1 [20].
Our data support a tumour suppressor mechanism for BRCA1; somatic mutations and LOH may result in inactivation of BRCA1 in at least a small number of ovarian cancers [21].
The BRCA1 gene on chromosome 17q21 is responsible for an autosomal dominant syndrome of increased susceptibility to breast and ovarian cancer but no somatic mutations in tumours have yet been described [21].
PIK3CA is implicated as an oncogene in ovarian cancer [22].
Recent studies have suggested that the phenotype in BRCA1 families with respect to the ratio of breast to ovarian cancer varies with the location of the BRCA1 mutation [23].

Anatomical context of Ovarian Neoplasms

Clinical and pathological features of ovarian cancer in women with germ-line mutations of BRCA1 [24].
In addition, EEF1A2 expression made NIH3T3 fibroblasts tumorigenic and increased the growth rate of ES-2 ovarian carcinoma cells xenografted in nude mice [25].
T cells conditioned with the B7-H1-blocked MDCs had a more potent ability to inhibit autologous human ovarian carcinoma growth in non-obese diabetic-severe combined immunodeficient (NOD-SCID) mice [26].
CONTEXT: Lysophosphatidic acid (LPA) has been shown to stimulate proliferation of ovarian cancer cells and is present in the ascitic fluid of patients with ovarian cancer [27].
METHODS: VEGF expression was examined in a simian virus 40 T-antigen-immortalized ovarian surface epithelial cell line (IOSE-29) and in ovarian cancer cell lines (OVCAR-3, SKOV-3, and CAOV-3) treated with LPA [28].

Gene context of Ovarian Neoplasms

EMSY links the BRCA2 pathway to sporadic breast and ovarian cancer [1].
In addition, downstream effectors of PI3-kinase, AKT1 and AKT2, have been found to be amplified or activated in human tumours, including ovarian cancer [22].
Thus, EEF1A2 and the process of protein elongation are likely to be critical in the development of ovarian cancer [25].
Role of K-ras and Pten in the development of mouse models of endometriosis and endometrioid ovarian cancer [29].
BRCA1 and BRCA2 account for most cases of familial, early onset breast and/or ovarian cancer and encode products that each interact with hRAD51 [30].

Analytical, diagnostic and therapeutic context of Ovarian Neoplasms

We randomly assigned 410 women with advanced ovarian cancer and residual masses larger than 1 cm after initial surgery to receive cisplatin (75 mg per square meter of body-surface area) with either cyclophosphamide (750 mg per square meter) or paclitaxel (135 mg per square meter over 24 hours) [31].
Identification of BRCA1 should facilitate early diagnosis of breast and ovarian cancer susceptibility in some individuals as well as a better understanding of breast cancer biology [32].
Combination chemotherapy consisting of hexamethylmelamine and cisplatin, alone or with doxorubicin hydrochloride, was given to 27 patients with advanced ovarian cancer who had disease progression with therapy including alkylating agents [33].
OBJECTIVE--To assess whether tubal ligation and hysterectomy affect subsequent risk of ovarian cancer [34].
OBJECTIVE: To determine whether hormone replacement therapy using estrogen only, estrogen-progestin only, or both estrogen only and estrogen-progestin increases ovarian cancer risk [35].

References

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