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

Calcemic alterations in prostate cancer are extremely rare. Hypercalcemia may be seen in cases of multiple osseous dissemination, and even in the absence of this in response to humoral mechanisms. The existence of hypercalcemia may indicate tumoural recurrence, and may at times be a datum prior to the diagnosis of the tumour. In cases of disseminated prostate adenocarcinoma hormones treatment may secure the normalization of blood calcium. We present a case of prostate carcinoma diagnosed in a 76-year-old patient, as a result of the presentation of a hypercalcemic metabolic syndrome, which was corrected after treatment by means of complete androgenic blocking.
 ...
PMID:[Hypercalcemia: a finding indicative of a prostatic adenocarcinoma]. 253 67

Obesity is an essential risk factor for hypertension, coronary heart disease and stroke as well as for metabolic disturbances, especially for type 2 diabetes, hyper- and dyslipidemia, and it is responsible for the metabolic syndrome with insulin resistance and hyperinsulinemia. Disturbances in the lung function are also induced by obesity, as a higher risk for arthrosis on the lower extremities. Some oncological diseases like breast-, endometrial-, and prostatic cancer are associated with obesity. It is evident, that the fat distribution plays an important role in the development of obesity associated diseases: the accumulation of visceral fat has a higher risk as the peripheral fat, probably due to the different metabolism.
 ...
PMID:[Obesity: entrance port to multimorbidity]. 988 99

The purpose of the present study was to perform a BPH risk factor analysis in men, relating the prostate gland volume to components of the metabolic syndrome and to identify clues to the etiology of BPH. Our material comprised a consecutive series of 158 patients with lower urinary tract symptoms with or without manifestations of the metabolic syndrome. In this group, the measured volume of the prostate was related consecutively to potential risk factors. The diagnoses atherosclerosis, non-insulin-dependent diabetes mellitus (NIDDM) and treated hypertension were obtained from the patient's medical history. Data on blood pressure, waist and hip measure, body height and weight were collected and body mass index (BMI) and waist/hip ratio (WHR) were calculated. Blood samples were drawn from fasting patients to determine insulin, cholesterol, triglycerides, HDL and LDL-cholesterol, uric acid and ALAT. The prostate gland volume was determined using ultrasound. Our results show that there was a larger prostate gland in men with NIDDM (P=0.0058), treated hypertension (P=0.0317), obesity (P<0.0001), low HDL-cholesterol levels (P=0.0132) and high insulin levels (P<0.0001) than in men without these conditions. The prostate gland volume correlated positively with the systolic blood pressure (r(s)=0.17; P=0.03), obesity (r(s)=0.34; P<0.0001) and fasting insulin (r(s)=0.38; P<0.0001) and negatively with HDL-cholesterol (r(s)=-0.22; P=0.009). On the basis of our findings, we concluded that NIDDM, treated hypertension, obesity, low HDL-cholesterol levels and high insulin levels constitute risk factors for the development of BPH. The results suggest that BPH is a facet of the metabolic syndrome and that BPH patients may share the same metabolic abnormality of a defective insulin-mediated glucose uptake and secondary hyperinsulinemia as patients with the metabolic syndrome. The findings generate a hypothesis of a causal relationship between high insulin levels and the development of BPH. In a clinical setting, the findings of the present report suggest that, in any patient presenting with BPH, the possible presence of NIDDM, hypertension, obesity, high insulin and low HDL-cholesterol levels should be considered. Conversely, in patients suffering from these conditions, the possibility of a clinically important BPH should be kept in mind.
Prostate Cancer Prostatic Dis 1998 Mar
PMID:Components of the metabolic syndrome-risk factors for the development of benign prostatic hyperplasia. 1249 10

The issue of a possible relationship between type 2 diabetes and cancer is still debated. Such chronic diseases show a high incidence in the general population. In their pathophysiology both genetic and environmental factors are involved, inducing important modifications of metabolism. Diabetes is associated to profound metabolic alterations, such as hyperinsulinemia and insulin resistance, which are common in various diseases, i.e. obesity, hypertension, dyslipidemia and hyperuricemia. Those illnesses form the so-called metabolic syndrome. Insulin resistance, hyperestrinism and the associated hyperandrogenism may play a role in the onset of some malignancies, such as endometrium cancer, breast cancer and prostate cancer. Low plasma levels of IGF-1 are able to reduce the risk of cancer in type 2 diabetes patients. This goal can be obtained with preventive measures, as physical activity, diet and drugs that can reduce insulin resistance (metformin and thiazolidinediones).
 ...
PMID:Evidence for a putative relationship between type 2 diabetes and neoplasia with particular reference to breast cancer: role of hormones, growth factors and specific receptors. 1503 27

Metabolic syndrome was initially described as an aggregation of risk factors for the development of coronary artery disease with insulin resistance and compensatory hyperinsulinemia as the underlying factor. In an earlier review, we suggested that hyperinsulinemia may also lead to prostate cancer (PCa), the most common male cancer in industrialized nations. Furthermore, we suggested that diet and exercise, known to be important in the development of insulin resistance, may also be important in the development of PCa. When we placed men from the United States on a low-fat diet and/or exercise program, serum levels of insulin, free testosterone, estradiol and insulin-like growth factor (IGF)-1 were reduced while sex hormone-binding globulin (SHBG) and insulin-like growth factor binding protein (IGFBP)-1 were elevated. These in vivo serum changes directly impacted on androgen-dependent prostate cancer cell lines in vitro to reduce cell growth and induce apoptosis. The reduction in serum IGF-1 and increase in IGFBP-1 with diet and exercise appear to be the most significant, as these changes lead to an increase in tumor cell p53 protein and its down-stream effector p21, which are responsible for the reduction in cell growth and induced apoptosis. Preliminary results from a clinical study with men on "watchful waiting" indicate that the observed in vitro effects of diet and exercise on prostate cancer cell growth also occur in vivo.
 ...
PMID:Preclinical models relevant to diet, exercise, and cancer risk. 1564 82

Adiponectin, a major adipose cytokine, plays a crucial role in the inhibition of metabolic syndrome by acting on such cell types as muscle cells and hepatocytes. Furthermore, evidence suggests that adiponectin may influence cancer pathogenesis. Adiponectin occurs in non-proteolytic (full-length adiponectin: f-adiponectin) and proteolytic (globular adiponectin: g-adiponectin) forms in various oligomeric states. Different forms of adiponectin show distinct biological effects through differential activation of downstream signaling pathways. Here we identify c-Jun NH(2)-terminal kinase (JNK), and signal transducer and activator of transcription 3 (STAT3) as common downstream effectors of f- and g-adiponectin. f- and g-adiponectin both stimulate JNK activation in prostate cancer DU145, PC-3, and LNCaP-FGC cells, hepatocellular carcinoma HepG2 cells, and C2C12 myoblasts. Furthermore, both f- and g-adiponectin drastically suppress constitutive STAT3 activation in DU145 and HepG2 cells. These suggest that JNK and STAT3 may constitute a universal signaling pathway to mediate adiponectin's pathophysiological effects on metabolic syndrome and cancer.
 ...
PMID:Adiponectin activates c-Jun NH2-terminal kinase and inhibits signal transducer and activator of transcription 3. 1593 15

Previous studies have suggested that hyperinsulinaemia and other components of metabolic syndrome are risk factors for clinical prostate cancer. This prospective study tested the hypothesis that hyperinsulinaemia and other components of metabolic syndrome are risk factors for lethal clinical prostate cancer. The clinical, haemodynamic, anthropometric, metabolic and insulin profile at baseline in men who had died from clinical prostate cancer during follow-up was compared with the profile of men who were still alive at follow-up. If the hypothesis is true, men with an unfavourable prognosis would have a higher profile at baseline than those with a favourable prognosis. A total of 320 patients in whom clinical prostate cancer, stages T2-3, had been diagnosed were consecutively included in the study during 1995-2003. Height, body weight, waist measurement, hip measurement and blood pressure were determined. Body mass index and waist/hip ratio (WHR) were calculated. Blood samples were collected to determine triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, uric acid, alanine aminotransferase and fasting plasma insulin level. The prostate gland volume was measured using transrectal ultrasound. The annual benign prostatic hyperplasia (BPH) growth rate was calculated. The diagnosis of prostate cancer was established using transrectal ultrasound-guided automatic needle biopsy of the prostate gland. All patients with clinical prostate cancer were followed up until their death or until the study was terminated on 31 December 2003. At follow-up, 54 patients had died from prostate cancer and 219 were still alive. The results showed that the men who died of clinical prostate cancer during the follow-up period were older (P < 0.001), had a larger prostate gland volume (P < 0.001), a faster BPH growth rate (P < 0.001), a higher prevalence of type 2 diabetes (P < 0.035) and treated hypertension (P < 0.023), a higher stage (P < 0.001) and grade (P = 0.028) of clinical prostate cancer, a higher prostate-specific antigen (PSA) level (P < 0.001) and a higher PSA density (P < 0.001) at baseline than men still alive with clinical prostate cancer at follow-up. These men also had a lower HDL-cholesterol level (P = 0.027), a higher fasting plasma insulin level (P = 0.004), a higher WHR (P = 0.097) of borderline significance and a higher uric acid level (P = 0.079) of borderline significance. Eliminating the effect on mortality of higher stage and grade of the clinical prostate cancer and PSA at baseline, the following statistically significant correlations remained: a higher fasting plasma insulin level (P = 0.010) and a lower HDL-cholesterol level of borderline significance (P = 0.065). In conclusion, hyperinsulinaemia and five other previously established components of metabolic syndrome are shown to be prospective risk factors for deaths that can be ascribed to prostate cancer. These findings confirm previous study, which indicate that prostate cancer is a component of metabolic syndrome. Moreover, these data indicate that hyperinsulinaemia and other metabolic disorders precede deaths caused by prostate cancer. Thus, our data support the hypothesis that hyperinsulinaemia is a promoter of clinical prostate cancer. Furthermore, our data suggest that the insulin level could be used as a marker of prostate cancer prognosis and tumour aggressiveness, regardless of the patient's prostate cancer stage, cancer grade and PSA level.
 ...
PMID:Hyperinsulinaemia: a prospective risk factor for lethal clinical prostate cancer. 1624 13

The aim of the study was examination of cause-effect relationships between PADAM, extragonadal production of androgens and high proliferative activity in aged men. The study group included 15 patients aged between 53 and 79 years with prostatic cancer (n = 5), urinary bladder cancer (n = 5) and cancer of the rectum (n = 5). Control samples of tissues of the prostatic gland, urinary bladder and rectum were obtained from dead bodies of men at the age between 18 and 29 years killed in the accidents at the age from 18 to 29 years. Testosterone levels in the tissues of peritumor zone of the prostate, in tumor tissue of patients with cancer of the prostate, urinary bladder and the rectum were higher than in blood serum. In prostatic cancer, testosterone in the tumor tissue was higher than in the tissues of prostatic peritumor zone. The values of Histochemical score AR of the peritumor zone in prostatic cancer patients were higher than those of the control group. It was detected that ER, PR, bcl-2, Ki-67 and p53 in prostatic tissue of young controls were absent while in patients with prostatic cancer these factors were expressed in the peritumor zone. In cancer of the urinary bladder, peritumor zone showed expression of PR, bcl-2, Ki-67 and p53, while no such expression was in the controls. ER, bcl-2, Ki-67 and p53 were registered in the peritumor zone of patients with cancer of the rectum but the controls had neither ER, bcl-2 nor p53 while Ki-67 expression in rectal cancer was higher than in the controls. The results of the study suggest that testosterone production by some tumors and tissues of the peritumor zone accompanied with high proliferative activity and dysregulation of the cell cycle is secondary to PADAM. These changes arise to compensate testicular deficiency and are manifestations of metabolic syndrome (X-syndrome). In this situation immune system fails to utilize all atypical cells.
 ...
PMID:[Testosterone production by tumor tissue in partial androgen deficiency in aged men (PADAM)]. 1628 38

Prostate cancer, the third most common cancer in men worldwide, varies substantially according to geographic region and race/ethnicity. Obesity and associated endocrine variation are foremost among the risk factors that may underlie these regional and ethnic differences. The association between obesity and prostate cancer incidence is complex and has yielded inconsistent results. Studies that have linked obesity with prostate cancer mortality, advanced stage disease, and higher grade Gleason score, however, have produced more consistent findings, indicating that obesity may not necessarily increase the risk of prostate cancer, but may promote it once established. Additionally, metabolic syndrome, which includes disturbed glucose metabolism and insulin bioactivity, may also be associated with prostate carcinogenesis. Adipokines, defined as biologically active polypeptides produced by adipose tissue, have been linked with a number of carcinogenic mechanisms, including angiogenesis, cell proliferation, metastasis, and alterations in sex-steroid hormone levels. A number of emerging studies have implicated the role of adipokines in prostate carcinogenesis. This review explores the specific roles of several adipokines as putative mediating factors between obesity and prostate cancer with particular attention to leptin, interleukin-6 (IL-6), heparin-binding epidermal growth factor-like growth factor (HB-EGF), vascular endothelial growth factor (VEGF) and adiponectin.
 ...
PMID:Obesity, adipokines, and prostate cancer (review). 1646 80

The relationship between obesity and prostate cancer is currently a hotly debated topic, but despite the number of publications devoted to the topic, the actual nature of the relationship remains uncertain. Obesity has been shown to have a direct relationship with the incidence of prostate cancer in a number of studies but an equal number of studies have shown no association. The relationship is further obscured with recent findings that obesity in younger obese men may actually be protective against prostate cancer. Confounding factors include the lack of correlation of body mass index (BMI) as a measure of central obesity and the lack of consistency in timing of BMI measurements, i.e. before or after diagnosis and in young or advanced adulthood. Evidence for increased BMI as a risk factor for prostate cancer is unclear, but less ambiguous is the mounting substantiation that obesity is associated with prognostically worse disease, poorer post-surgical outcomes and increased prostate cancer mortality, irregardless of margin status. From a biologic perspective, one can put forth a number of potential mechanisms by which obesity might promote prostate cancer and/or prostate cancer progression including; low levels of testosterone, increased levels of estrogen, co-existing diabetes or metabolic syndrome, increased circulating insulin-growth factor-one (IGF-1), increased levels of leptin, decreased levels of adiponectin and increased dietary saturated fats. Evidence for the association of these factors with prostate cancer are examined herein. The timing of serum measurements is crucial in elucidating whether these factors have causative influence on prostate cancer or rather are produced by the prostate cancer cells and are better understood as markers of disease. The interaction between obesity and prostate cancer is important to clarify because it will have impact on the prevention, prognostication and treatment of prostate cancer. Future study with careful attention to avoid the methodological pitfalls of the past need be accomplished to bear out the nature of the interaction of obesity and prostate cancer.
 ...
PMID:Obesity and prostate cancer. 1667 23


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