Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 89 subjects including 30 breast cancer patients with distal metastases, 29 patients with benign breast disease, and 30 healthy subjects were studied. Serum samples from these subjects were obtained from the National Cancer Institute (NCI) Breast Cancer Serum Bank, Bethesda. Serum concentrations of vitamin A and its transport proteins (prealbumin and retinol-binding protein [RBP]), beta-carotene, vitamin E, and selenium were determined. For each of these parameters the mean for the breast cancer patients was lower than that of the healthy subjects. The differences between healthy subjects and patients with either breast cancer or benign breast disease were, however, statistically significant only in the case of RBP (p less than 0.05). In the case of vitamin A and its transport proteins these differences were reduced by comparing the cancer patients with the benign breast disease patients rather than with the healthy controls. This indicates that the low serum levels for those three parameters may be merely a consequence of disease in general rather than a feature of cancer per se.
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PMID:Serum vitamins A and E, beta-carotene, and selenium in patients with breast cancer. 262 Dec 91

Different mechanisms have been proposed to explain the rapid elimination of circulating malignant cells: interactions with circulating leukocytes, mechanical trauma induced by deformation, shear forces and tissue pressure variations. Based on earlier observations in an isolated heart perfusion model the present study was performed to test whether or not microvascular damage of malignant cells depends on their anti-oxidant status. Murine melanoma B16F10 cells, pretreated with 100 microM alpha-tocopherol (or solvent) for 48 h, were used. The cells were perfused into the coronary vasculature of isolated hearts from C57/BL6 mice. Passing cells were collected and their viability determined by Trypan Blue exclusion. The hearts were processed for electron microscopy and the frequency of ultrastructurally intact and damaged B16 cells trapped in capillaries was recorded. In filter perfusion experiments the effect of vitamin E pretreatment on the resistance of the melanoma cells to mechanical deformation was determined. Morphometrically, cell size and cell profile perimeter excess of the melanoma cells were computed. Vitamin E pretreatment increased perfused cell viability from 50% to 81%. Ultrastructurally 30% of the intracapillary vitamin E treated cells were damaged (plasmalemmal fragmentation or worse) as compared to 58% of control cells. These differences were statistically significant (P < 0.01) whereas no differences could be demonstrated in filterability, cell size, or cell surface excess. The data support the hypothesis that malignant cell destruction in the systemic microcirculation is at least partly dependent on an oxygen metabolite mediated process, the exact nature (e.g. superoxide, hydrogen peroxide, nitric oxide) of which remains to be determined.
Clin Exp Metastasis 1995 Jul
PMID:Melanoma cell destruction in the microvasculature of perfused hearts is reduced by pretreatment with vitamin E. 760 89

We report about one case of spontaneous healing of metastases of kidney cancer (hypernephroma). The subcutaneous and abdominal metastases appeared 3 years after the discovery of the initial neoplasm and subsequent nephrectomy. Meanwhile the patient developed an adenoma of the prostate, while the neoplasm was in a metastasizing stage. After prostatectomy, he was treated with Ephynal for mild transient incontinence. From then on, we witnessed progressive disappearance of the metastases, until they were completely eradicated. This case is very well documented, with irrefutable histological evidence of the nature of the lesions and of their healing. It adds to the 21 similar cases published worldwide until then. In recent cases, the beneficial role of vitamin D in the treatment of metastases of kidney cancer has been predicted. We have probably demonstrated accidentally that vitamin E, which has some similarities with vitamin D, is a least as effective. In addition, it is a particularly innocuous and cheap medication. This may be an interesting therapeutic improvement, considering that there is no really effective treatment of metastasized kidney cancer, except very heavy Interleukin-based therapies that are both very expensive and hard to bear for the patient.
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PMID:[Spontaneous recovery from metastatic cancer of the kidney. Favourable role of Vitamin E?]. 816 3

Severity of prognosis factors in breast cancer cases was found to be associated with an increase in plasma vitamin E and a decrease in plasma malondialdehyde (peroxidability index). The first aim of this study was to determine whether this association is also present in other cancers. Measurements were taken before therapy on 129 patients with various carcinomas. Cholesterol was also investigated, as vitamin E is closely related to this analyte. Patients were classified by tumor size (T < or = 5 cm and T > 5 cm) and by invasion status, assessed by the presence of nodes and/or metastasis. The vitamin E/total cholesterol concentration ratio was higher and the cholesterol and malondialdehyde concentrations were significantly lower in the plasma of patients with large tumors or in whom nodes and/or metastasis were present, whatever the site. The multivariate analysis performed to measure the association of these analyte concentrations with tumor progression showed that the presence of nodes and/or metastases was inversely associated with a low vitamin E/total cholesterol ratio (OR, 0.5; CI, 0.3-1.1) and, directly associated with low plasma concentrations of cholesterol and malondialdehyde (OR, 3.0; CI, 1.3-6.8 and OR, 2.8; CI, 1.2-6.7 respectively). The same types of associations were identified with large tumors, but were less strong. Together these findings supported an alteration of lipid parameters related to the oxidant-antioxidant status in cancer patients. This alteration appears to be associated with tumor growth and progression in patients with various cancer sites.
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PMID:Tumor progression and oxidant-antioxidant status. 868 41

Prostate cancer is the most common human malignancy and the second leading cause of cancer deaths among men in Western nations. Descriptive epidemiologic data suggest that androgens and/or environmental exposures, such as diet (in particular, dietary fat), play an important role in prostatic carcinogenesis. One plausible link between diet and prostate cancer is oxidative stress. This process refers to the generation of reactive oxygen species, which can then trigger a host of pro-carcinogenic processes. Recent studies also indicate that androgens increase oxidative stress within human prostate cancer cell lines. Recent data from our institution indicate that oxidative stress is higher within the benign epithelium of prostate cancer patients than men without the disease. This confirms our hypothesis and suggests that antioxidants such as lycopene, vitamin E, and selenium may play an important role in preventing disease progression. Large-scale clinical trials with some of these agents are currently in the design phase.
Cancer Metastasis Rev
PMID:Diet, androgens, oxidative stress and prostate cancer susceptibility. 1045 75

Chemoprevention is prevention of cancer by administering natural or synthetic chemicals. Anti-androgens are among the promising chemopreventive agents for prostate cancer because prostate epithelium is androgen dependent. A National Cancer Institute supported large, randomized, clinical prostate cancer chemoprevention trial has been conducted to test the efficacy of finasteride, an inhibitor of 5-a-reductase, which converts testosterone to 5-hydroxy-testosterone. Now the focus is on micronutrients and phytochemicals, which have potential preventive effects against prostate cancer. Lycopene, soy isoflavones, vitamin E and selenium are among the most promising nutritional chemopreventive agents. Another NCI supported large clinical chemoprevention trial was recently started to investigate the efficacy of selenium and vitamin E, alone or in combination in the prevention of prostate cancer. Inclusion of appropriate biomarkers in clinical trials will help elucidate the mechanisms by which genetic and epigenetic pathways of carcinogenesis are modulated by nutrients and phytochemicals.
Cancer Metastasis Rev 2002
PMID:Chemoprevention of prostate cancer. 1246 50

The selection of micronutrients, defined as essential and nonessential dietary components consumed in minute quantities, for testing in clinical chemoprevention trials is based on the totality of evidence arising from epidemiologic, in vitro, animal, and clinical studies. Those micronutrients that surface with chemopreventive potential, in terms of high efficacy and low toxicity, in early-phase clinical studies are then candidates for large-scale, randomized clinical chemoprevention trials with cancer endpoints. Micronutrients currently being examined in National Cancer Institute (NCI)-sponsored phase I, II, or III chemoprevention trials for prostate, breast, and colon cancers include isoflavones, lycopene, selenized yeast, selenomethionine, selenium, vitamin E, perillyl alcohol, folic acid, vitamin D, calcium, and curcumin. The response to micronutrients may vary not only in magnitude but also in direction. This variation and response likely depend on individual genetic polymorphisms and/or interactions among dietary components that influence absorption, metabolism, or site of action. Research priorities include investigation of possible molecular targets for micronutrients and whether genetic and epigenetic events dictate direction and magnitude of the response.
Cancer Metastasis Rev 2002
PMID:Micronutrients in cancer chemoprevention. 1254 62

Lung cancer is the leading cause of cancer death in the United States. The current mainstays of lung cancer therapy are surgery, radiation and chemotherapy. These interventions have produced slight declines in mortality rates in the last 5 years however, it appears unlikely that marked improvements will occur in the near future. This grim overview argues strongly for new, emerging approaches for controlling this disease. Chemoprevention is the use of specific natural or synthetic substances with the objective of reversing, suppressing or preventing carcinogenic progression to invasive cancer. Whether primary, secondary or tertiary settings, prevention has the highest potential to improve the dismal statistics associated with this cancer. Several randomized clinical or translational chemoprevention trials have been conducted. All have so far produced either neutral or harmful primary endpoint results showing that lung cancer was not prevented by alpha-tocopheral, beta-carotene, retinal, retinyl palmitate, N-acetylcysteine or isotretinoin in smokers. Secondary results supporting treatment with isotretinoin in 'never' and former smokers and data from prevention trials involving selenium and vitamin E however, are encouraging and offer a promising direction for future clinical study. Other areas of promise for future lung cancer chemoprevention study include the study of molecular markers of risk and drug activity, molecular targeting study, improved imaging techniques and new drug delivery systems.
Cancer Metastasis Rev 2002
PMID:Chemoprevention of lung cancer: current status and future prospects. 1254 71

The Ewing sarcoma is the second most common bone tumor in children and young adults. Despite the advances in therapy, the 5-year survival rate for patients with metastatic disease is poor, indicating the need for alternative treatments. Here, we report that 2-methoxy-estradiol (2-Me), a natural estrogen metabolite, induced a caspase-dependent apoptosis of Ewing sarcoma-derived cells independently of their p53 status. 2-Me-induced apoptosis occurred through the mitochondrial death pathway as evidenced by reduction of the mitochondrial transmembrane potential, cytochrome c release and caspase-9 activation. Treatment of cells with 2-Me resulted in generation of intracellular H(2)O(2), which occurred earlier than caspase-9 activation. The H(2)O(2)-reducing agent Ebselen and the lipid peroxidation inhibitor vitamin E decreased both 2-Me-induced caspase-9 activation and cell death, thus providing evidence for a role of H(2)O(2) and lipid peroxides in the initiation of this process. Rotenone, an inhibitor of the mitochondrial respiratory chain, abolished both apoptosis and H(2)O(2) production, thereby identifying mitochondria as the source of H(2)O(2). Moreover, we observed that treatment of cells with 2-Me or H(2)O(2) induced activation of the c-Jun N-terminal kinase (JNK). Overexpression of a dominant-negative mutant of JNK1 reduced 2-Me-induced apoptosis indicating that JNK participates in this process. Altogether, our results provide evidence that 2-Me triggers apoptosis of Ewing sarcoma cells through induction of a mitochondria redox-dependent mechanism and suggest that this compound or other agents that selectively increase the level of reactive oxygen species may prove useful to the development of novel strategies for treatment of Ewing tumors.
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PMID:2-Methoxyestradiol induces apoptosis in Ewing sarcoma cells through mitochondrial hydrogen peroxide production. 1273 Jun 70

RRR-alpha-tocopheryl succinate (alpha-vitamin E succinate, VES), one of the vitamin E derivatives, can effectively inhibit the proliferation of human prostate cancer cells. However, little is known about its effect on prostate cancer cell invasive ability. Tumor metastasis is a complex process and the extracellular matrix (ECM) is the first barrier that tumor cells encounter. Therefore, we tested the effect of VES on the invasion of different prostate tumor cells, PC-3, DU-145, and LNCaP, through Matrigel, a reconstituted ECM, using an in vitro cell invasion assay. The invasion of PC-3 and DU-145 cells through Matrigel was inhibited by 20 microM VES after treating for 24 h. The condition did not alter cell survival, cell cycle, cell adhesion or cell motility. We further investigated whether the ability of VES to inhibit prostate cancer cell invasiveness was associated with its ability to inhibit the activity of matrix metalloproteinases (MMPs), the key enzymes in the proteolysis of basement membrane during invasion. PC-3 and DU-145 cells that were treated with VES showed a significant reduction in the levels of MMP-9 in the culture medium. In contrast, LNCaP cells, which did not secrete MMP-9, were poorly invasive in Matrigel and were hardly affected by treatment with VES. This is the first report suggesting that VES inhibits human prostate cancer cell invasiveness and the reduction of secreted MMP-9 activity could be one of the contributory factors, which points to the potential use of VES in the prevention and therapy of prostate cancer invasion.
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PMID:RRR-alpha-tocopheryl succinate inhibits human prostate cancer cell invasiveness. 1504 90


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