Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case history of a patient who developed mammary cancer (T1N1bMo) after 5 1/2 years of continuous treatment with Levodopa for Parkinson's disease is presented. The prolactin inhibition by the Levodopa was verified, and the clinical and mammographic growth, the doubling time, and the labeling index of the tumor were determined. The results were not significantly different than those obtained from patients with breast cancer not under treatment with Levodopa. The rapid growth and evolution of this tumor suggests that prolactin does not have an inducer or promoter effect in mammary cancer.
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PMID:Breast cancer in a patient under levodopa treatment. 67 56

Family histories of male patients with histologically confirmed malignant gliomas were compared to family histories of controls (wives). Included were 77 case families with 892 relatives and 77 control families with 719 relatives. Cases had significantly more siblings than controls (P = 0.02), although cases were not preferentially the oldest or the youngest sibs. Odds ratios of two or more were found for mental retardation, Parkinson's disease, and meningitis for the relatives of cases versus controls, but none were statistically significant. The excesses of Parkinson's disease and meningitis were explained by the family of one particularly interesting case containing three relatives with meningitis and two relatives with Parkinson's disease. Noteworthy age-adjusted odds ratios for cancer among relatives of cases compared to relatives of controls were 1.6 (95% confidence interval (CI) = 1.0-2.3) for cancer of any site, 2.4 (95% CI = 0.8-6.1) for breast cancer, and 4.0 (95% CI = 0.6-10.7) for lung cancer. Only the odds ratio for cancer of any site was statistically significant. Overall, 6 of 77 (8%) of cases came from families that included two or more relatives with breast or lung cancer in addition to the proband with malignant glioma. These three cancer sites may form familial clusters worthy of further evaluation in future studies by pedigree and genetic linkage analyses.
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PMID:Familial factors associated with malignant gliomas. 222 74

Dopamine agonists have been indicated as treatment for disorders such as Parkinson's disease, cardiogenic shock and dopamine insufficiency. A unique relationship exists between dopamine and carcinogenicity. Chronic prolactin stimulation has been identified as a promoter of carcinogenicity. Prolactin secretion is regulated through dopamine receptor activation. Dopaminergic agonists inhibit prolactin release and antagonists increase release. High levels of prolactin have been shown to suppress production of estrogen and progesterone. As a result of these findings, a series of experiments were designed to examine the effects of a specific dopamine agonist, SKF 38393, against MCF-7 cells. MDA-MB231 and MCF-10 cells were used as negative controls. The breast cancer in vitro screening procedure involved the plating of MCF-7, MDA-MB231 and MCF-10 cells in a 96-well plate assay. After 1 day, the cells were exposed to SKF 38393 for 2 days and cell growth was determined by the Alamar blue dye reagent method. The optical density data was analyzed and IC50 values determined. The results indicated that SKF 38393 caused a significant decrease in proliferation of MCF-7 cells. The IC50 value was 0.1 +/- 0.03 microM. The results also indicated no significant effect on MDA-MB231 and MCF-10 cells.
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PMID:The growth inhibitory properties of a dopamine agonist (SKF 38393) on MCF-7 cells. 767 Jan 47

This paper proposes a prenatal seasonal hypopigmentation influence associated with anomalous cerebral dominance that occurs during the winter or early spring. A possible mechanism would be seasonal changes in sex hormone levels that affect the activation and inactivation of DNA by reversible methylation. The proposed prenatal seasonal hypopigmentation effect might be relevant to dyslexia, Prader-Willi syndrome, breast cancer, Alzheimer's and Parkinson's disease. Putative chromosomal loci associated with the proposed seasonal mechanism would be 15q11-13 (dyslexia and Prader-Willi syndrome), 21q region (breast cancer and Alzheimer's disease) and 19p region (pigmentation gene).
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PMID:Hypopigmentation, anomalous cerebral dominance and seasonality. 818 25

Apoptosis, often synonymously used with the term 'programmed cell death', is an active, genetically controlled process that removes unwanted or damaged cells. Suppression, overexpression or mutation of a number of genes which orchestrate the apoptotic process are associated with disease. The diseases in which apoptosis has been implicated can be grouped into 2 broad groups: those in which there is increased cell survival (i.e. associated with inhibition of apoptosis) and those in which there is excess cell death (where apoptosis is overactive). Diseases in which there is an excessive accumulation of cells include cancer, autoimmune disorders and viral infections. Deprivation of trophic factors is known to induce apoptosis in cells dependent on them for survival. This fact has been exploited in the use of antiandrogens or antiestrogens in the management of prostate or breast cancer. Haemopoietic growth factors like granulocyte-macrophage colony stimulating factor (GM-CSF) or interleukin-3 prevent apoptosis in target cells and modulation of levels of these factors has been tried in the prevention of chemotherapy-induced myelosuppression. Until recently, it was thought that cytotoxic drugs killed target cells directly by interfering with some life-maintaining function. However, of late, it has been shown that exposure to several cytotoxic drugs with disparate mechanisms of action induces apoptosis in both malignant and normal cells. Physiological regulation of cell death is essential for the removal of potentially autoreactive lymphocytes during development and the removal of excess cells after the completion of an immune response. Recent work has clearly demonstrated that dysregulation of apoptosis may underlie the pathogenesis of autoimmune diseases by allowing abnormal autoreactive lymphocytes to survive. AIDS and neurodegenerative disorders like Alzheimer's or Parkinson's disease represent the most widely studied group of disorders where an excess of apoptosis has been implicated. Amyotrophic lateral sclerosis, retinitis pigmentosa, epilepsy and alcoholic brain damage are other neurological disorders in which apoptosis has been implicated. Apoptosis has been reported to occur in conditions characterised by ischaemia, e.g. myocardial infarction and stroke. The liver is a site where apoptosis occurs normally. This process has also been implicated in a number of liver disorders including obstructive jaundice. Hepatic damage due to toxins and drugs is also associated with apoptosis in hepatocytes. Apoptosis has also been identified as a key phenomenon in some diseases of the kidney, i.e. polycystic kidney, as well as in disorders of the pancreas like alcohol-induced pancreatitis and diabetes.
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PMID:Apoptosis: clinical relevance and pharmacological manipulation. 933 59

Investigators have hypothesized that occupations involving electric and magnetic field exposure are associated with a variety of health problems, including neurological disease. The authors conducted a case-control study, and they used U.S. death certificates with occupational coding to compare male cases of Alzheimer's disease (n = 256), Parkinson's disease (n = 168), and amyotrophic lateral sclerosis (n = 114) with controls matched for age and calendar time. The authors selected controls in a 3:1 ratio to cases from persons who died of causes other than leukemia, brain cancer, and breast cancer. Overall associations with electrical occupations were modest (i.e., adjusted odds ratios of 1.2, 1.1, and 1.3 for Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, respectively). Individual electrical occupations were associated more strongly with disease than overall electrical occupations, particularly amyotrophic lateral sclerosis, for which relative risks ranged from 2 to 5 across several job categories. The largest associations with all three diseases occurred for power plant operators.
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PMID:Electrical occupations and neurodegenerative disease: analysis of U.S. mortality data. 957 Mar 11

To investigate the risks of mortality and cancer incidence in Parkinson's disease (PD) we studied the prognosis of 246 PD patients in a community. The cohort of PD patients was identified in 1984, and survival, mortality, relocation, and cancer incidence during 1984-1992 were examined retrospectively in 1994. The risk was measured by a standard effect estimate, i.e., the standardized mortality ratio (SMR) or the standardized incidence ratio (SIR), compared with the rates in the general population. During the observation period 696 person-years in PD men and 1018 person-years in PD women were accumulated, and 49 PD men and 53 PD women died. The risk of mortality in PD was significantly increased in both sexes (SMR: men 1.74, women 1.97). In addition, the risk of cancer incidence was evaluated in 228 patients aged under 80 years; 8 PD men and 7 PD women developed cancer. The risk of overall cancer incidence in PD was less than 1 in either sex, but not significantly. The risk of breast cancer in PD women was significantly increased (SIR: 5.49), but the 95% confidence interval was wide (1.10-16.03). The results indicate that PD patients in a community have a twofold higher risk of mortality, and that PD may be associated with an increased risk of breast cancer in women.
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PMID:Mortality and cancer incidence in patients with Parkinson's disease. 1092 71

The effects of 17beta-estradiol and the anti-estrogen, tamoxifen, on methamphetamine-induced neurotoxicity of the nigrostriatal dopaminergic system were examined in ovariectomized CD-1 mice. In Experiment 1, striatal dopamine concentrations from estrogen treated mice were significantly greater than that from non-estrogen treated mice following methamphetamine. Dopamine concentrations from estrogen+tamoxifen+methamphetamine treated mice were decreased compared to estrogen+methamphetamine treated mice and not significantly different from those of tamoxifen+methamphetamine treated mice or mice receiving methamphetamine alone. These results suggest that estrogen is functioning as a neuroprotectant of methamphetamine-induced nigrostriatal dopaminergic neurotoxicity and that this neuroprotective effect of estrogen is abolished in the presence of tamoxifen. In Experiment 2, estrogen administration after methamphetamine treatment did not produce any significant changes in dopamine concentrations compared with methamphetamine treatment alone. The data from Experiment 2 show that estrogen cannot reverse the methamphetamine-induced neurotoxicity upon the nigrostriatal dopaminergic system. Similar results were observed for the potassium-stimulated dopamine outputs from these treatment conditions as evaluated with in vitro superfusion, although a difference between the two measures for the estrogen+methamphetamine treated group was obtained in Experiment 1. These results have important implications for estrogen-tamoxifen interactions upon the nigrostriatal dopaminergic system and the gender differences which are observed in Parkinson's disease and animal models of nigrostriatal dopaminergic neurotoxicity as well as for the proposed use of tamoxifen in pre-menopausal women at risk for breast cancer.
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PMID:Tamoxifen abolishes estrogen's neuroprotective effect upon methamphetamine neurotoxicity of the nigrostriatal dopaminergic system. 1124 53

Estradiol is a pleiotropic hormone, involved in the etiology of a wide variety of diseases. Over the last decade individual genetic variability of the estradiol metabolism has been described as a significant contributor to disease susceptibility with variations depending on ethnic background. Among others, genetic variations of genes encoding cytochrome P450 (CYP) enzymes play an important role in this regard. Mutant alleles of the CYP 1A1 gene are major modulators of lung cancer risk among smokers, mediate gender differences in lung cancer susceptibility, and have been associated with an elevated risk for breast, prostate, colorectal, and oral squamous cell cancer. Variants of the CYP 1B1 gene modulate the risk for prostate, ovarian, lung, and breast cancer. Also, mutations in the CYP 1B1 gene are the major genetic determinant of congenital glaucoma. Mutant CYP 17 alleles are associated with serum and plasma levels of steroid hormones, use of hormone replacement therapy, and endometrial, prostate, and breast cancer. Available data indicate that the protective effect of a later age at menarche is limited to mutant CYP 17 allele carriers. Among women with the Polycystic Ovary (PCO) syndrome, mutant CYP 17 alleles are sufficient to aggravate the clinical presentation of the disease. Molecular variants of the CYP 19 gene are associated with an increased risk for breast cancer, advanced disease stage, and tumor aromatase production. Carriage of a mutant catechol-O-methyltransferase (COMT) allele is associated with breast cancer, neurologic disorders such as Parkinson's disease, and modulates behavior among patients with schizophrenia, alcoholics and the general population. In summary, the available evidence points to estrogen metabolising genes as strong hereditary determinants of the susceptibility to benign and malignant conditions.
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PMID:Genetic modeling of estrogen metabolism as a risk factor of hormone-dependent disorders. 1195 95

Estradiol is a pleiotropic hormone, involved in the etiology of a wide variety of diseases. Over the last decade individual genetic variability of the estradiol metabolism has been described as a significant contributor to disease susceptibility with variations depending on ethnic background. Among others, genetic variations of genes encoding cytochrome P450 (CYP) enzymes play an important role in this regard. Mutant alleles of the CYP 1A1 gene are major modulators of lung cancer risk among smokers, mediate gender differences in lung cancer susceptibility, and have been associated with an elevated risk for developing breast, prostate, colorectal, and oral squamous cell cancer. Variants of the CYP 1B1 gene modulate the risk for developing prostate, ovarian, lung, and breast cancer. Also, mutations in the CYP 1B1 gene are the major genetic determinant of congenital glaucoma. Mutant CYP 17 alleles are associated with serum and plasma levels of steroid hormones, use of hormone replacement therapy, and the development of endometrial, prostate, and breast cancer. Available data indicate that the protective effect against breast cancer of a later age at menarche is limited to wild-type CYP 17 allele carriers. Among women with the polycystic ovary syndrome, carriage of mutant CYP 17 alleles is sufficient to aggravate the clinical presentation of the disease. Molecular variants of the CYP 19 gene are associated with an increased risk for developing breast cancer, advanced breast cancer stages, and tumor aromatase production. Carriage of a mutant catechol-O-methyltransferase allele is associated with breast cancer, neurologic disorders such as Parkinson's disease, and modulates behavior among patients with schizophrenia, alcoholics and the general population. In summary, the available evidence points to genes that encode estrogen-metabolizing enzymes as strong hereditary determinants of the susceptibility to benign as well as malignant conditions.
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PMID:Genetic modelling of the estrogen metabolism as a risk factor of hormone-dependent disorders. 1202 Sep 74


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