Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C1140680 (ovarian cancer)
 28,141 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have shown that platinum-DNA adduct level in leukocyte DNA (measured by antibody methodology) is directly related to disease response in ovarian cancer and testicular cancer. To determine if this principle could be more broadly applied, platinum-DNA damage was studied in a blinded fashion in leukocyte DNA of 21 cancer patients who received carboplatin (day 1) and cisplatin (day 3) in a phase 1 clinical trial. Fifteen different tumor types were included in this cohort. Using atomic absorption spectrometry with Zeeman background correction, DNA-bound platinum was measured during cycles 1 (C1) and 2 (C2) of therapy for most patients. For each of two cycles of therapy, most patients developed measurable levels of adduct after carboplatin, and in most patients adduct levels increased further after cisplatin, often in a supra-additive fashion. Total mg dose levels varied by less than 2-fold, whereas individual patients differed by as much as 10(3) in their adduct measurements after C1 and after C2, and by 29-fold after the very first carboplatin dose. All patients had refractory disease at the initiation of therapy, and 19 patients were evaluable for disease response. Adduct determinations were made 24 h after the first dose of platinum therapy in 17 of these individuals. Mean adduct levels after the first dose of carboplatin were higher in six responders (50 fmol/micrograms DNA +/- 26) than in 11 non-responders (14 fmol/micrograms DNA +/- 10); Wilcoxon two sample test two-sided P = 0.0071. The six responders were patients with pleural mesothelioma (2), breast cancer, buccal mucosa cancer, esophageal cancer and ovarian cancer. Adduct levels were consistently higher in the group of responders on each day that adduct was measured, with a summary two-sided P value of 0.00011. We conclude that analysis of platinum-DNA adduct formation may help determine whether pharmacogenetics are important in cancer drug resistance; and may help to determine the relationship between DNA damage in the peripheral blood compartment and internal organ response to in vivo exposures to DNA-damaging agents.
Carcinogenesis 1991 Jul
PMID:Platinum-DNA damage in leukocyte DNA of patients receiving carboplatin and cisplatin chemotherapy, measured by atomic absorption spectrometry. 207 Apr 90

From an overview of epidemiological evidence on nutrition, diet and cancers of the breast, endometrium and ovary, the following indications can be drawn: Overweight and obesity are causally related to endometrial and post-menopausal breast cancer, and may account for as much as one third of the cases of endometrial and one tenth of breast cancer in Europe. It is not known whether obesity or overweight early in life has any role on breast cancer risk, nor whether obesity influences ovarian carcinogenesis. Overweight tends to be associated with an unfavourable prognosis for breast cancer. Despite extensive research, the available knowledge on diet and breast cancer is largely inconsistent, and the results from ecological and individual-based studies are contradictory in relation to fat, proteins, total energy, alcohol, etc. There are only scanty data on diet and endometrial or ovarian cancer, which tend to suggest role for fat (or animal fat) in the risk of these neoplasms. The evidence on diet and breast, ovarian and endometrial carcinogenesis is still too scanty or inconsistent to be of any practical preventive value. Thus, the only clear indication for prevention is that a reduction of overweight would avoid a substantial number of cases of endometrial and post-menopausal breast cancer.
 ...
PMID:Nutritional factors and cancers of the breast, endometrium and ovary. 269 10

The biochemical responses to 8-week supplementary treatment with selenium and/or vitamin E were evaluated in 41 patients with gynaecological cancer during cytotoxic chemotherapy, in Finland, a selenium-deficient country. After the control course of 1-day treatment with cytostat agents, 11 patients received a combination of selenium and vitamin E (sodium selenate, 200 micrograms/day + vitamin E, 300 mg/day), 11 received selenium (sodium selenate, 200 micrograms/day) and seven received vitamin E (300 mg/day) as supplementary therapy, while 12 patients had no supplementary drugs. Sodium selenate alone and combined with vitamin E significantly increased the serum selenium levels, but the activity of serum glutathione peroxidase (GSH-Px) increased significantly only in the selenium- and vitamin E-treated patients with low initial GSH-Px activity. The cytotoxic chemotherapy did not change the activity of GSH-Px, while the concentrations of lipid peroxides decreased. Sodium selenate alone or with vitamin E did not modify this decrease. Sodium selenate alone significantly decreased the capacity of the platelets to produce thromboxane A2; it increased high-density lipoprotein cholesterol levels and prevented the cytotoxic-chemotherapy-associated increase of creatine kinase. Selenium supplementation might thus be beneficial during cytotoxic chemotherapy in ovarian cancer patients with low selenium levels.
Carcinogenesis 1989 Feb
PMID:Supplementation with selenium, vitamin E and their combination in gynaecological cancer during cytotoxic chemotherapy. 291 78

The question of whether the steroidal components in oral contraceptives (OCs) may have an initiating or promotional influence on the development of cancer continues to be raised as a public health issue. It is estimated that since the introduction of OCs nearly 25 years ago, more than 150 million women have used 1 or more types of the formulation and nearly 1 billion woman-years of exposure to the steroids have accumulated. Contraceptive practice in Australia would indicate that about 25% of women of reproductive age are using OCs. The debate about the OC's carcinogenic potential has recently been reopened with 2 reports in "The Lancet" of an association between the incidence of breast and cervical cancer and OC usage. Biologically the relationship between the contraceptive steroids and cancer must continue to be regarded as the most important concern with the longterm use of OCs. The demonstration of receptors to these steriods in these organs, in both normal and malignant tissues, further increases the speculation that the steroid hormones have a biological role in carcinogenesis in these target organs. Theoretical reasons exist for the concern about carcinogenesis and contraceptive steroids. This paper reviews the available evicence. Data can be derived only from large-scale epidemiological research, by means of case-control or cohort studies. No clear evidence exists that OCs cause or increase the chance of developing any cancer in the female genital tract and the breast. In fact, OC offers a significant protection against the development of endometrial and ovarian cancer, especially to those women who have taken OCs for a long time. The association between the risk of breast cancer and OC use is less certain, but factors such as the history of benign breast disease, a close relationship with breast cancer, or nulliparity -- previously considered to be important -- do not appear to contribute significantly to the risk. The weight of evidence indicates that no increased risk of breast cancer exists, even in those younger women aged less than 25 years who decide to use OCs before their 1st full-term pregnancy. There is some evidence that suggests that the risk of cervical neoplasia -- dysplasia, carcinoma-in-situ and invasive carcinoma -- may increase slightly in OC users but the actual part played by the patient's sexual history under these circumstances remains to be defined. There is now strong evidence to implicate multiplicity of sexual partners and wart virus infection in carcinogenesis of the uterine cervix. There does not appear to be an overall relationship between OCs and malignant melanoma. Overall, the evidence is reassuring. The low-dose combined OC can be considered safe, not only in terms of cardiovascular and thromboembolic risks, but also in relation to carcinogenesis.
 ...
PMID:Cancer risks and the contraceptive pill. What is the evidence after nearly 25 years of use? 351 57

A familial form of ovarian carcinoma is now widely recognized. There are at least several ovarian cancer-prone genotypes, consistent with genetic heterogeneity. Prophylactic oophorectomy has been employed for women who were judged to be at 50% risk for this disease by virtue of their position in the pedigree. However, recent evidence has disclosed that a fraction of such patients who underwent prophylactic oophorectomy and who had ovaries which appeared to be histologically normal at surgical resection, subsequently developed intraabdominal carcinomatosis with histologic findings showing the lesions to be indistinguishable from ovarian carcinoma. Given the embryologic derivatives of the ovary, which comprise gonadal ridges composed of mesodermal cells covered by coelomic epithelium, we postulate that patients with hereditary predisposition to ovarian carcinoma harbor the first germinal hit in both the epithelial cells of the ovary as well as their derivatives in the coelomic mesothelium. These patients may then be inordinately susceptible to carcinogenesis from the second (somatic) hit in these same tissues.
 ...
PMID:Familial peritoneal ovarian carcinomatosis: a new clinical entity? 364 Oct 31

To explore the relationships between the antioxidant selenium and pro-aggregatory thromboxane A2 in patients with gynaecological cancer, we measured the serum concentrations of selenium and the production of thromboxane B2 (TxB2, a stable metabolite of thromboxane A2) by the aggregating platelets in patients with endometrial (n = 35), ovarian (n = 30) and cervical cancer (n = 25), and in 32 control women. The selenium concentration in endometrial (1.14 +/- 0.04 mumol/l; mean +/- SE), ovarian (0.96 +/- 0.04 mumol/l) and cervical cancer (0.97 +/- 0.06 mumol/l) was significantly lower than in control subjects (1.26 +/- 0.03 mumol/l). The release of TxB2 into serum during spontaneous clotting of the blood was significantly increased in ovarian cancer (229.2 +/- 15.9 ng/ml), decreased in endometrial cancer (142.6 +/- 12.4 ng/ml) and normal in cervical cancer (185.9 +/- 14.8 ng/ml) as compared with control subjects (185.9 +/- 11.9 ng/ml). The levels of selenium and TxB2 did not correlate with each other in the whole series or in any subgroup. Thus, selenium does not seem to be an important determinant in the biosynthesis of TxB2 in patients with gynaecological malignancy.
Carcinogenesis 1986 Jul
PMID:Serum selenium and thromboxane in patients with gynaecological cancer. 371 1

Serum concentrations of selenium were determined by atomic absorption spectrophotometry in 40 patients with ovarian cancer in association with and after surgical and cytostatic therapy. Patients with ovarian cancer had significantly (p less than 0.001) lower serum concentrations (mean +/- SE) of selenium (0.93 +/- 0.04 mumol/l) than age-, weight- and place of residence-matched control subjects (1.22 +/- 0.03 mumol/l). In clinical stage IV disease there was a lower serum level of selenium (0.82 +/- 0.07 mumol/l) than in clinical stages I and II combined (1.00 +/- 0.04 mumol/l). Serum selenium concentrations also showed a tendency to follow the outcome of the disease; an increase in patients with remission and a decrease in patients with progressive disease, probably because of nutritional reasons.
Carcinogenesis 1984 Jun
PMID:Serum selenium in patients with ovarian cancer during and after therapy. 642 13

The ovarian cancer risk from herbicide exposure has been studied in a hospital-based, case-control study after some of these compounds have been shown to be carcinogenic for animals. This study includes 60 cases of primary mesothelial ovarian tumors and 127 controls with non-ovarian malignancies drawn from the same file and matched by year of diagnosis, age and residence. A positive association (relative risk 4.38) has been found between herbicide exposure and ovarian mesotheliomas.
Carcinogenesis 1984 Jul
PMID:Ovarian mesothelial tumors and herbicides: a case-control study. 673 55

The Food and Drug Administration (FDA), in agreement with the recommendations of its Fertility and Maternal Health Drugs Advisory Commite, concluded that there appears to be no increased risk of breast cancer in oral contraceptives (OC) users or any subgroup of users, or with any particular type of OC. However, the FDA is concerned that there may be an increased risk of cervical carcinoma among OC users. Since the introduction of OCs, many investigations have been conducted to address their possible relationship to carcinogenesis. Studies have demonstrated that OCs appear to have a protective effect against ovarian and endometrial cancer. The risk for ovarian cancer has been found to be lower among all OC users than among nonusers. The longer a woman used OCs, the lower her risk of ovarian cancer, and the lower risk persisted after OC use had stopped. The protective effect against endometrial cancer was observed only with the combination OCs containing both an estrogen and progestogen. A greater risk of endometrial cancer was reported in women taking sequential pills, which are no longer marketed in the US. An increased risk of breast cancer in longterm use before age 25 of combination type OCs with a "high" progestogen content and an increased risk of cervical carcinoma in OC users compared with IUD users have been reported. In November 1983 the National Institute of Child Health and Human Development convened a meeting to discuss the findings of the breast cancer study. Questions were raised specifically about the use of the delay of menses test as the sole basis for ranking progestogen potency, the accuracy of telephone interviews, and the possibility of age differences in cases and controls. Other studies were also reviewed. The findings of the breast and cervical cancer studies were also presented to FDA's Fertility and Maternal Health Drugs Advisory Committee in February 1984. Although the data from the cervical cancer study may be confounded by sexual activity, smoking, and other variables, the FDA concluded that there may be an increased risk of cervical carcinoma among OC users. Women taking OCs should be monitored carefully with physical examinations and Pap tests, at least yearly. The FDA also recommends that OCs with the lowest effective dose of estrogen be used. For any given estrogen-progesogen combination, it is advisable to use that product which contains the lowest doses of estrogen and progestogen consistent with the needs of the patient.
 ...
PMID:Oral contraceptives and cancer. 673 89

The total duration of 'ovulatory activity' or 'ovulatory age' has been reported to be the strongest indicator of the risk of ovarian cancer. In the case-control study examined in this paper this variable was found to be a strong correlate of the risk of ovarian cancer. However, the finding that in older women the major determinant of 'ovulatory age' was age at menopause (which is a very unreliable indicator of 'ovarian activity'), and that age at menopause by itself was related to the risk of ovarian cancer as strongly as the total duration of ovulatory age, threw doubt on the biological consistency of that model. Furthermore, the protection conferred by pregnancies was different at different ages, and age at first pregnancy was more strongly associated with the risk of ovarian cancer than the actual number of pregnancies. The model of carcinogenesis for epithelial ovarian cancer appears, therefore, to be more complex than is indicated simply by the total duration of 'ovarian activity.'
 ...
PMID:Incessant ovulation and ovarian cancer: a critical approach. 687 10


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>