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Query: UMLS:C1140680 (ovarian cancer)
 28,141 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiple genome alterations can be seen within a tumor and continue to accumulate throughout development of the growth. Chromosome deletions occurring in tumors are generating much interest. To date, the best known model is retinoblastoma whose study gave rise to the concepts of anti-oncogene or tumor suppressor gene. Studies of genetic anomalies in colorectal tumors have led to an elegant model of colonic carcinogenesis in which multiple steps, each with its corresponding genetic anomaly, successively accumulate, with deletion of the p53 gene occurring as a late event. Successive anomalies of the p53 gene (mutations, deletions) occur during passage from a low-grade astrocytoma to a higher-grade astrocytoma. Studies of familial forms of breast cancer and of breast and ovarian cancer have also provided insight into the biology of these tumors, with the identification of a predisposing chromosomal area whose location is 17 q-12-21. These approaches open up possibilities for screening techniques and use of preventive treatments in highly selected patients. However they raise many ethical problems. There is a need for developing a charter for these family studies in the near future.
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PMID:[Genetics and cancers]. 130 91

Manganese superoxide dismutase (Mn-SOD) is strongly expressed in human ovarian cancer, and the serum level of the enzyme is a useful marker for the diagnosis and monitoring of human ovarian cancer. In the present study we found that Mn-SOD was highly expressed in primary and transplanted ovarian cancers in rats induced by 7,12-dimethylbenz[a]anthracene (DMBA), as judged by enzyme-linked immunosorbent assay as well as by Northern blot analysis. The serum levels of Mn-SOD in the tumor-bearing rats were also higher than those in control rats. The antibody strongly reacted with rat ovarian carcinoma tissues. These data suggest that DMBA-induced ovarian cancer in rats is a good experimental model for human ovarian cancer, and that Mn-SOD is also a good marker for disease in the animal model.
Carcinogenesis 1992 Oct
PMID:High expression of manganese superoxide dismutase in 7,12-dimethylbenz[a]anthracene-induced ovarian cancer and increased serum levels in the tumor-bearing rats. 142 60

We compared the hormonal and epidemiological aspects of ovarian cancer patients in search of the etiology of this neoplasia. Case-control studies of Japanese women with and without cancer were conducted in parallel, with regard to both the excretion of 14 urinary steroids and the pertinent physical and physiological parameters. The results obtained are as follows: 1) premenopausal ovarian cancer patients before and after radical ovariectomy and postmenopausal-postoperative patients were associated with a specified steroid deviation profile characterized by a combination of general depression of androgens, progestins and corticosteroids with sole rescue of tetrahydrocortisol (THF) in urine. 2) The deviation profile of postmenopausal-preoperative cancer patients was distinguished from the 3 partner profiles by its preservation of normalcy in the excretions of androgen and progestin in urine. 3) Ovarian cancer patients were associated with growth retardation, when compared with urban healthy controls and patients with either breast cancer or endometrial cancer by the age-matching method. Ovarian cancer patients were also less fertile than age-matched normal controls, and were as infertile as age-matched patients with either breast cancer or endometrial cancer. 4) Epidemiological evidence was presented to suggest that the incidence of ovarian cancer in Japan was increasing in parallel with the recent increase of social tension in Japan. The possible relevance of the hormonal characteristics of ovarian cancer patients to both the epidemiological characteristics of the same cancer patients and the genesis of this neoplasia is discussed in the light of the 2-step carcinogenesis theory.
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PMID:Relation between the hormonal and epidemiological aspects of ovarian cancer patients in Japan. 144 27

The epidemiologic data collected to date have provided some important and provocative clues as to the etiology of ovarian cancer. The recognition of familial clustering of this disease has led to exciting advances in understanding the genetics involved. The contribution of endocrine factors has been well documented in the epidemiologic literature, leading to important insights into the process of carcinogenesis. Clearly, additional information is needed to further explain the interplay of genetic, physiologic, and life style factors, to lead to a better understanding of the disease, and ultimately to a means of prevention and control.
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PMID:The epidemiology of ovarian cancer. 150 Mar 82

We have constructed deletion maps of chromosome 3p for cancers of the female genital tract (uterine endometrium, uterine cervix and ovary). The tumours were tested for loss of heterozygosity using CA-repeat polymorphisms. The high degree of informativeness of these markers allowed the construction of detailed deletion maps from a relatively small number of samples. A common region of deletion was identified at chromosome 3p13-21.1 in endometrial cancer and at 3p13-14.3 in cervical cancer; 5 out of 13 (38%) endometrial cancers and six out of eight (75%) cervical cancers showed loss of heterozygosity at these regions. In ovarian cancer a separate common region of deletion was identified at 3p21.1-22; two out of four (50%) ovarian cancers had alleles deleted at this region. These data suggest the presence of a tumour-suppressor gene(s) for endometrial and cervical cancer at 3p13-21.3 and a separate gene at 3p21.1-22 that is involved in the carcinogenesis of ovarian cancer.
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PMID:Deletion mapping of chromosome 3p in female genital tract malignancies using microsatellite polymorphisms. 163 Aug 22

In an effort to analyze molecular mechanisms of human ovarian carcinogenesis, we studied the structure and expression of the p53 gene in different cell lines established from human ovarian carcinomas. In all six lines (PA-1, Caov-3 and -4, OVCAR-3, SK-OV-3, and Kuramochi), p53 abnormalities were detected. In the SK-OV-3 cell line, Southern analysis suggested the presence of sequence deletions/rearrangements in at least one allele of the p53 gene, and transcripts were not detectable by either Northern or polymerase chain reaction analysis. Sequence analysis of the entire coding region of the p53 gene revealed point mutations resulting in codon changes of a highly conserved region of the protein in four cell lines, Caov-3 and -4, OVCAR-3, and Kuramochi. In the Caov-3 cell line, the point mutation resulted in chain termination at codon 136. Quantitation of p53 protein by immunoprecipitation analysis revealed a 6-fold higher than control cell level in PA-1. By contrast, p53 protein was not detectable in lines Caov-3 and SK-OV-3. We conclude that altered levels of p53 gene expression and/or mutant forms of the p53 gene product are associated with all human ovarian cancer cells tested.
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PMID:Abnormal structure and expression of the p53 gene in human ovarian carcinoma cell lines. 163 34

This review of the action of estrogens and progestagens, the steroids in oral contraceptives, on cells in the endometrium, breast, ovary, cervix and other tissues, regarding possible causative role in cancer development focuses on the level of steroid receptors and observed actions of these hormones on the cellular level. The steroid hormones are thought to interact with cells by binding to a specific receptor on the cell surface, especially estrogen receptors, while progestagen receptors overlap with glucocorticoids and androgens. Oral contraceptives typically have progestin dosages at the plateau of the dose-response curve, but lower estrogen doses may possible improve the cancer risk. Plasma levels are not reliable estimates of estrogen influence; moreover, estrogens are synthesized locally. Carcinogenesis is a multi-stage process requiring cell proliferation, involving an initiating event, and probably promotion agents, resulting in tumor growth. Estrogens increase cell replication in endometrium, and progestins counter it. Breast cancer evolves in several cell types in the epithelium of the terminal ductal lobular unit, with a 20-year latency. Estrogens stimulate ductal growth and progestins its development, and both are required for full stimulation, as in pregnancy. Estrogens usually stimulate cancer growth, but the precise sensitivity to steroids depends on the timing in the life cycle of the tumor. Ovarian cancer is unique in that neoplasms arise from the epithelium, not the hormone-sensitive tissue. Therefore the suppressive effect of steroids on ovarian neoplasia is thought to be via down- regulation of the gonadotropins, prevention of follicular rupture and consequent cell division of the epithelium, or some effect on growth regulating factors. The effect of steroids on the cervix is unclear, since cervical cancers are hormone-resistant, but there may be a step in transformation by human papilloma virus that involves a glucocorticoid- or progesterone receptor. Steroid receptors are also known to exist in tumors of liver, skin, colon, kidney and anterior pituitary, but their function is neoplasia is unknown.
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PMID:Biology of female sex hormone action in relation to contraceptive agents and neoplasia. 165 Dec 4

The relationship between use of oral contraceptives (OCs) and other contraceptive methods and the risk of ovarian cancer was examined in a combined analysis of 3 hospital-based case-control studies conducted in Italy, the United Kingdom, and Greece, for a total of 971 ovarian cancer cases and 2,258 controls under age 65. Compared with never-users, the combined multivariate relative risk (RR) for ever-users was 0.6 (95% confidence interval, CI = 0.4-0.8) and the estimates were consistent in the 3 datasets. The protection was also similar across strata of age and parity. Considering various measures of OC use, available in the Italian and British datasets only, the protection conveyed on ovarian cancer risk increased with the duration of use and persisted in the medium-long period: the RR in women reporting their last OC use greater than or equal to 15 years prior to diagnosis was 0.5 (95% CI = 0.2-1.0). The risks in ever-users were appreciably lower in those women who reported their first OC use before 25 years of age (RR = 0.3 for first use before age 25, 0.8 for first use at age 25-34 and 0.7 at 35 years or after). Such findings emerged similarly from Italian and British data. This combined analysis, besides offering further quantitative estimates of the protective effects of OCs on ovarian cancer risk in European populations, provides useful insights into the time pattern of the relationship between OC use and ovarian carcinogenesis, suggesting that the protection persists for 15 years or more after cessation of use and may be larger for use at younger age.
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PMID:Pooled analysis of 3 European case-control studies of epithelial ovarian cancer: III. Oral contraceptive use. 187 72

The descriptive and analytical epidemiology of ovarian cancer is reviewed, starting from the substantial geographical differences, with high rates in North America and Europe and low rates in developing countries and Japan, although, on a worldwide scale, almost 50% of 140,000 total cases occur in developing countries. Over the past decades, incidence and mortality rates have remained approximately stable in high-risk areas, but have generally tended to rise in low-risk areas. In the past, ovarian cancer was more common in higher social classes, but sociocultural differences seem to have flattened off over recent decades. In etiological terms, the protection afforded by multiparity and oral contraceptive (OC) use is well established, with relative risks (RRs) of the order of 0.5 for multiparae and OC users. There is also consistent evidence that risk increases with late age at menopause. Less consistent and weak, if any, are the effects of age at menarche and first birth, although there is hint that a first birth over age 35 is not protective. It is conceivable that diet can play an important role in ovarian carcinogenesis, but only scattered data are available to suggest that high fat consumption may represent an indicator of risk. Available knowledge on ovarian cancer epidemiology is also discussed in relation to models of carcinogenesis and implications for prevention and public health.
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PMID:The epidemiology of ovarian cancer. 195 94

A series of in vitro and in vivo studies were performed to characterize DNA damage recognized by an antiserum elicited against DNA modified with cis-diamminedichloroplatinum(II) (cisplatin). Adducts determined by the cisplatin-DNA enzyme-linked immunosorbent assay (ELISA) in human blood cell DNA have been shown to correlate well with positive clinical outcome in testicular and ovarian cancer patients receiving platinum drug-based chemotherapy (Reed et al. (1990) Proc. Natl. Acad. Sci., 84; 5024, and Reed et al. (1988) Carcinogenesis, 9, 1909). DNAs from calf thymus, salmon sperm, pBR322 and synthetic oligonucleotides were modified with cisplatin in vitro before or after specific DNA digestion steps to yield adducted samples of known size and/or chemical composition. These cisplatin modified DNAs were assayed by atomic absorption spectrometry (AAS) to assess absolute platinum content, and by ELISA to determine the antiserum specificity. The antiserum recognizes native cisplatin-modified calf thymus DNA, and native oligonucleotides containing intrastrand cis-Pt (NH3)2-d(pGpG) adducts (Pt-GG) and intrastrand cis-Pt (NH3)2-d(pApG) adducts (Pt-AG). Modified plasmid DNA fragments of varying sizes (down to 309 base pairs) are recognized similarly to cisplatin-modified calf thymus DNA. The antiserum does not cross-react with individual Pt-GG or Pt-AG adducts not bound to DNA. In experiments designed to assess the relationship between adduct measured by ELISA and total platinum bound to DNA as measured by AAS, male and female Sprague-Dawley rats were injected i.p. with cisplatin and a dose response for adduct formation was determined in kidney DNA samples. Values obtained by ELISA were substantially lower than those measured by AAS, and the two were directly related in DNA from kidney tissues of rodents but not in DNA from human nucleated blood cells. In rodent samples the ELISA measured a consistent 0.2% of the total DNA-bound platinum determined by AAS, with a correlation coefficient of 0.91. Among 54 blood cell DNA samples from human patients, which gave measurable adduct values in both ELISA and AAS, the ELISA measured a variable fraction (0.2-33.0%) of the total DNA-bound platinum measured by AAS. We conclude that the cisplatin-DNA ELISA measures a three dimensional lesion in DNA that is formed in direct proportion to total DNA-bound platinum in rat kidney, but that in human biological samples, interindividual variability precludes a relationship that conforms to simple mathematical algorithms.
Carcinogenesis 1990 Dec
PMID:Characterization of the DNA damage recognized by an antiserum elicited against cis-diamminedichloroplatinum (II)-modified DNA. 197 37


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