Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A complex of investigation was performed in 30 males with newly diagnosed prostatic cancer (stages T2NOMO-T3NO-1MO) before treatment with estrogens, 2-3 months and 1 year after its start. The complex included evaluation of blood lipid spectrum (HDL, LDL, VLDL, triglycerides), hemostasis (coagulation, platelet aggregation, fibrinolysis), hormonal profile (blood hydrocortisone, aldosterone, testosterone, estradiol, STH, FSH, LH, prolactin, plasma renin activity), central and intracardiac hemodynamics, ECG. 66 healthy men of advanced age served control. It was found that estrogen therapy affected blood lipid metabolism, leading to impairment of physiological correlation between HDL and triglycerides, increased blood levels of VLDL and triglycerides. Long-term estrogen treatment brought about enhancement of hemocoagulation and platelet aggregation. Hormonal shifts involved hyperprolactinemia, hypersomatotropism, hypercorticism, aldosterone hypersecretion, proportional androgens-estrogens alterations. Hormonal abnormalities produce side effects in estrogen-treated CHD and hypertonic patients: negative ECG readings indicative of deteriorated coronary circulation and hypertensive episodes, central hemodynamic disorders, respectively. In view of possible cardiovascular damage related to estrogen therapy, a differentiated approach is proposed which would allow a long-term estrogen treatment free of relevant complications.
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PMID:[The assessment of the state of the blood lipid spectrum, hemostasis, hormonal homeostasis and hemodynamics in the early diagnosis and drug correction of the cardiovascular changes in prostatic cancer patients undergoing estrogen therapy]. 141 45

This review discusses the molecular mechanism of the regulation of prostate growth, maintenance of the prostate integrity and possible disturbances in these processes leading to the development of prostatic cancer and benign hyperplasia. The role of hormones, growth factors, oncogenes is described in more details. The participation of the angiotensin converting enzyme and renin-angiotensin systems in the regulation of polyamine synthesis in the prostate and the regulation of prostate growth is assumed.
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PMID:[Regulation of prostatic growth, pathogenesis of prostatic adenoma and cancer]. 753 May 31

Prolyl oligopeptidase (EC 3.4.21.26) activity was measured in human tissue homogenates and body fluids. The enzyme was ubiquitously present, revealing high activity in renal cortex, epithelial cells, fibroblasts, testis, lymphocytes and thrombocytes. The activity in the body fluids was low. Prolyl oligopeptidase activity was significant higher in tumours of prostate, lung and sigmoid, than in the healthy tissues. Sera of individuals suffering from HIV infection, malaria, prostate cancer or benign prostate hypertrophy contained lowered activity. Interestingly, the low serum activity during prostate carcinoma increased upon medical treatment with anti-androgens. This suggests hormonal control of the gene transcript. A positive correlation with angiotensin converting enzyme activity in hypertensive patients was demonstrated and this further supports the possible involvement of prolyl oligopeptidase in the renin-angiotensin system and in the pathogenesis of hypertension.
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PMID:Distribution of prolyl oligopeptidase in human peripheral tissues and body fluids. 870 29

Hypokalemic paralysis is a medical emergency due to the risks of cardiac arrhythmia, respiratory failure, and rhabdomyolysis. Besides supplementing patients with KCl to hasten recovery, the astute physician must search for the underlying cause to avoid missing a treatable and curable disorder. We report on an elderly Korean man who presented with marked limb paralysis, myalgias, and mild hypertension. He had prostate cancer treated with orchiectomy and hormone therapy 2 years previously. The major biochemical abnormalities were hypokalemia (K+: 1.7 mmol/l) associated with high renal K+ wasting and metabolic alkalosis (HCO3-: 42.6 mmol/l). Low plasma renin activity, low aldosterone concentration, and normal cortisol concentration pointed to a state of pseudohyperaldosteronism. While reviewing his drug history, the patient revealed he had been consuming eight packs (100 ml/pack) of a Korean herbal tonic daily to treat his prostate cancer for the past 2 months. A significant amount of glycyrrhizic acid (0.23 mg/ml), an active ingredient of licorice, was detected in the tonic. Discontinuation of the herbal tonic along with KCl supplementation achieved recovery in 2 weeks. As many complementary/alternative medicines for cancer contain licorice, this must be kept in mind as a cause of hypokalemia in cancer patients.
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PMID:A hidden cause of hypokalemic paralysis in a patient with prostate cancer. 1535 80

Our previous study demonstrated that Angiotensin II (Ang-II) which is well known to be a main peptide of the renin-angiotensin system could activate the cell proliferation of prostate cancer as well as EGF, and an Ang-II receptor blocker(ARB) could inhibit it through the suppression of phosphorylation of MAPK and STAT3. Also, ARB exerted an antiproliferative effect on prostate cancer through paracrine factors from stromal cells. We believe that ARBs have the novel ability to suppress the development or progression of prostate cancer. Furthermore, based on the idea that inhibition of G protein-coupled receptor signaling in cancer and stromal cells could suppress prostate cancer growth, a novel treatment such as molecular targeting therapy to overcome this devastating disease could be possible in the future.
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PMID:[Novel molecular targeting therapeutics for prostate cancer]. 1571 89

An apparent low prevalence of cancer in hypertensive patients receiving angiotensin converting enzyme inhibitors is reported; however, the molecular mechanisms have not been elucidated. Angiotensin-II (Ang-II) is well known to be associated with hypertension, as a main peptide of the renin-angiotensin system, and its detailed molecular mechanisms have recently been elucidated. For instance, Ang-II directly activates the mitogenic signal transduction pathway through the angiotensin-II type-1 (AT1) receptor in smooth muscle cells and cardiac myocytes. Ang-II receptor blockers (ARBs), a class of antihypertensive agent, suppress signal transduction pathways mediated by growth factors such as epidermal growth factor (EGF), through the AT1 receptor. Our studies demonstrated that an ARB had the potential for antiproliferative effects and inhibition of angiogenesis in prostate cancer cells. The AT1 receptor is categorized in the guanosine phosphate binding protein-coupled receptors (GPCRs), which are viewed as critical regulators of the interactions between epithelial and stromal cells. Hence, we consider that in overcoming prostate cancer, it is very important to inhibit GPCR signaling in cancer cells by ARBs. It is unclear how prostate cancer growth changes from being hormone dependent to independent, and no effective therapy has therefore been developed. Our clinical data revealed that ARB administration decreased prostate specific antigen (PSA) and improved performance status in patients with hormone-refractory prostate cancer. This review provides an insight into the key role of Ang-II and the possibility of ARBs for molecular targeting of mitogenesis and angiogenesis in prostate cancer.
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PMID:Antiproliferative efficacy of angiotensin II receptor blockers in prostate cancer. 1610 80

It is known that the renin-angiotensin system (RAS) plays a fundamental role not only as a vasoconstrictor in controlling blood pressure and electrolyte/fluid homeostasis, but also as a mitogenic factor through the Ang-II type-1 (AT1) receptor in smooth muscle cells and cardiac myocytes. Angiotensin II (Ang-II) is indeed thought to be a growth factor, and Ang-II receptor blockers (ARBs), a class of antihypertensive agent, suppress signal transduction pathways mediated by several growth factors or cytokines, through the AT1 receptor. There is increasing evidence that the RAS is implicated in the development of various cancers. We previously demonstrated that ARBs have the potential to inhibit the growth of prostate cancer cells and tumors through the AT1 receptor. This review highlights the possibility of ARBs as novel agents for prostate cancer as well as other cancers, and reviews the literature on this area.
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PMID:Angiotensin II receptor blocker: possibility of antitumor agent for prostate cancer. 1684 33

Although a low prevalence of cancer in hypertensive patients receiving angiotensin converting enzyme inhibitors has been reported, the molecular mechanisms have not been elucidated. It is known that angiotensin-II (Ang-II) plays a fundamental role not only as a vasoconstrictor in controlling blood pressure and electrolyte and fluid homeostasis, but also as a mitogenic factor through the Ang-II type-1 (AT1) receptor in cardiovascular cells. Interestingly, there is increasing evidence that the renin-angiotensin system (RAS) is implicated in the development of various cancers. As we previously reported, AT1 receptor blockers (ARBs), a class of antihypertensive agent, have the potential to inhibit the growth of prostate cancer cells and tumors through the AT1 receptor. This review provides an insight into the key role of Ang-II and the AT1 receptor, and the possibility of ARBs for molecular targeting of mitogenesis and angiogenesis in prostate cancer.
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PMID:Pharmacology and new perspectives of angiotensin II receptor blocker in prostate cancer treatment. 1818 67

Angiotensin II has been shown to be a cytokine especially acting as a growth factor. A local renin-angiotensin system has been identified in the prostate gland, and the physiologic function of angiotensin II seems to be similar in prostate cancer, as we previously reported. In the present study, we explored the biological role of angiotensin II in oxidative stress of prostate cancer cells. Activated Akt was determined, and the expression of oxidative stress-related proteins (p47phox, manganese superoxide dismutase 2, glutathione peroxidase) was examined by Western blotting in LNCaP cells, which were stimulated with angiotensin II and/or an angiotensin II receptor type 1 blocker, candesartan. To examine DNA damage induced by angiotensin II, 8-hydroxy-2'-deoxyguanosine was determined, and Western blots were analyzed to detect checkpoint proteins including p53, Chk2, and cdc2. Immunocytochemical studies of inducible nitric oxide synthase and superoxide anion radical (O(2)(-)) were done in LNCaP cells stimulated with angiotensin II. The phosphorylation of Akt was induced by angiotensin II treatment and inhibited by candesartan, as well as by LY294002, an inhibitor of phosphoinositide 3-kinase. Oxidative stress-related proteins were up-regulated by angiotensin II and inhibited by pretreatment with candesartan or catalase. The level of 8-hydroxy-2'-deoxyguanosine was increased by angiotensin II and conversely decreased by candesartan. Immunocytochemical studies showed that angiotensin II enhanced an inflammatory marker, inducible nitric oxide synthase, and the production of O(2)(-) radical. The hypothesis that angiotensin II has the potential to induce oxidative stress, which may be implicated in carcinogenesis of the prostate gland through long-term exposure to chronic inflammation is proposed.
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PMID:Angiotensin II induces oxidative stress in prostate cancer. 1831 86

Prostate cancer is highly prevalent in Western society, and its early stages can be controlled by androgen ablation therapy. However, the cancer eventually regresses to an androgen-independent state for which there is no effective treatment. The renin-angiotensin system (RAS), in particular the octapeptide angiotensin II, is now recognised to have important effects on growth factor signalling and cell growth in addition to its well known actions on blood pressure, fluid homeostasis and electrolyte balance. All components of the RAS have been recently identified in the prostate, consistent with the expression of a local RAS system in this tissue. This review focuses on the role of the RAS in the prostate, and the possibility that this pathway may be a potential therapeutic target for the treatment of prostate cancer and other prostatic diseases.
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PMID:Role of the renin-angiotensin system in prostate cancer. 1882 67


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