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)

Hydrogen peroxide (H2O2) in nanomolar concentrations (20-100 nM) stimulated the growth of small (diameter 100 +/- 30 microm) multicellular prostate cancer spheroids and increased c-fos expression. H2O2 transiently raised [Ca2+]i by Ca2+ release from intracellular stores as the transient persisted in low (10 nM) Ca2+ solution but was abolished when intracellular Ca2+ stores were depleted by thapsigargin or chelation of [Ca2+]i with BAPTA. The H2O2-induced [Ca2+]i transient was furthermore inhibited by the P2-purinoreceptor antagonists suramin and basilen blue, indicating that H2O2 may act via purinergic receptor stimulation. Treatment of spheroids with either suramin, basilen blue or BAPTA inhibited the H2O2-induced growth stimulation and c-fos expression, indicating that the H2O2-mediated growth stimulation of multicellular spheroids is mediated via a Ca2+-dependent pathway.
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PMID:Calcium-dependence of hydrogen peroxide-induced c-fos expression and growth stimulation of multicellular prostate tumor spheroids. 942 34

Laboratory and clinical data indicate an antitumor effect of 1,25(OH)2 vitamin D (1,25(OH)2D) on prostate cancer. High calcium intake suppresses formation of 1,25(OH)2D from 25(OH)D, thereby decreasing the 1,25(OH)2D level. Ingestion of fructose reduces plasma phosphate transiently, and hypophosphatemia stimulates 1,25(OH)2D production. We thus conducted a prospective study among 47,781 men of the Health Professionals Follow-Up Study free of cancer in 1986 to examine whether calcium and fructose intake influenced risk of prostate cancer. Between 1986 and 1994, 1369 non-stage A1 and 423 advanced (extraprostatic) cases of prostate cancer were diagnosed. Higher consumption of calcium was related to advanced prostate cancer [multivariate relative risk (RR), 2.97; 95% confidence interval (CI), 1.61-5.50 for intakes > or = 2000 mg/day versus < 500 mg/day; P, trend, 0.002] and metastatic prostate cancer (RR, 4.57; CI, 1.88-11.1; P, trend, <0.001). Calcium from food sources and from supplements independently increased risk. High fructose intake was related to a lower risk of advanced prostate cancer (multivariate RR, 0.51; CI, 0.33-0.80, for intakes > 70 versus < or = 40 g/day; P, trend, 0.007). Fruit intake was inversely associated with risk of advanced prostate cancer (RR, 0.63; 95% CI, 0.43-0.93; for > 5 versus < or = 1 serving per day), and this association was accounted for by fructose intake. Non-fruit sources of fructose similarly predicted lower risk of advanced prostate cancer. A moderate positive association between energy-adjusted fat intake and advanced prostate cancer was attenuated and no longer statistically significant when controlled for calcium and fructose. Our findings provide indirect evidence for a protective influence of high 1,25(OH)2D levels on prostate cancer and support increased fruit consumption and avoidance of high calcium intake to reduce the risk of advanced prostate cancer.
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PMID:Calcium and fructose intake in relation to risk of prostate cancer. 945 87

A lower risk of prostate cancer among diabetics has been suggested by several but not all studies. However, the studies have not always accounted for time since diagnosis of diabetes mellitus, or have not examined confounding factors such as diet and diagnostic bias. We thus examined this relationship in the Health Professionals Follow-Up Study from 1986 and 1994, in which 1,369 new cases of non-stage A1 prostate cancer were documented in 47,781 men. A prior history of a diagnosis of diabetes (mostly adult-onset) was associated with a reduced risk of prostate cancer (multivariate relative risk [RR] = 0.75; 95 percent confidence interval [CI] = 0.59-0.95) controlling for age, body mass index (wt/ht2) at age 21, and, in 1986, race, vasectomy, and intakes of total energy, total fat, calcium, fructose, and lycopene. After excluding the first year of follow-up after the diagnosis of diabetes, the RR was 0.63 (CI = 0.54-0.89). Prostate cancer was not reduced in the first five years after diagnosis (RR = 1.24, CI = 0.87-1.77), but was lower in the next five years (RR = 0.66, CI = 0.39-1.10) and lowest after 10 years (RR = 0.54, CI = 0.37-0.78); P-value for trend across time = 0.004. Similar associations were noted for advanced cases. Detection bias was unlikely to account for our findings. The basis of this relationship is unclear but may reflect hormonal changes related to diabetes, perhaps low testosterone levels.
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PMID:Diabetes mellitus and risk of prostate cancer (United States). 948 58

We present a patient with prostate cancer who developed symptomatic hypocalcemia while taking oral clodronate for painful bony metastases. He had a past history of a bowel resection for Crohn's disease, and, although he was normocalcemic prior to taking clodronate, it is likely that the surgery had caused mild hyperparathyroidism. The addition of clodronate prevented the chronic osteolysis of bony metastases, which would have helped maintain normocalcemia. The case was complicated by hypomagnesemia and hypokalemia resulting from diarrhea. Hypomagnesemia is a cause of refractory hypocalcemia and hypokalemia. This case illustrates two important points. First, care must be taken with bisphosphonates in patients with a previous bowel resection. Second, magnesium plays a key role in the metabolism of both calcium and potassium, and must be considered in the evaluation of the hypocalcemic patient.
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PMID:Symptomatic hypocalcemia with oral clodronate. 949 15

The calcium-binding protein S100P has been found to be associated with human prostate cancer. We have overexpressed S100P in Escherichia coli using a T7 expression system. A rapid two-step procedure for the isolation of overexpressed S100P leads to a preparation of >95% pure protein with a yield of approximately 150 mg per liter of culture. The structural integrity of recombinant S100P was analyzed using CD and fluorescence spectroscopic techniques. The far-UV CD shows that secondary structure of recombinant S100P consists predominantly of a-helical structure. Both near-UV CD and tyrosine fluorescence spectra show that aromatic residues are involved in the formation of a specific, well packed structure, indicating that the recombinant S100P protein adopts a compact folded conformation. Ca2+ has a profound effect on S100P structure. Near-UV CD and fluorescence intensity of both internal (tyrosine) and external (ANS) probes suggest significant structural rearrangements in the tertiary structure of the molecule. The similarity of far-UV CD spectrum of S100P in the presence and in the absence of Ca2+ suggests that Ca2+ binding has only minor effects on secondary structure.
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PMID:Cloning, overexpression, purification, and spectroscopic characterization of human S100P. 951 77

Hypotonicity-induced Ca2+ signals and volume regulation were studied in proliferating and quiescent subpopulations of multicellular prostate cancer spheroids. Enzymatic dissociation of multicellular spheroids 100+/-19 microm in diameter, which are entirely proliferative, yielded a population of cells with a mean cell diameter of 17.5+/-1.4 microm. After dissociation of spheroids in a size class of 200+/-30, 300+/-60, and 400+/-65 microm in diameter, two subpopulations of cells with mean cell diameters corresponding to 12.9+/-1.9 microm and 16.7+/-2 microm were discriminated. The subpopulation of large cells was shown to be proliferative by positive Ki-67 antibody staining; the subpopulation of small cells was Ki-67 negative, indicating cell quiescence. In a spheroid size class of 100+/-19 microm, a distinct subpopulation of quiescent cells was absent. Superfusion by hypotonic solutions revealed that only the proliferating cell fraction showed a regulatory volume decrease (RVD) and a [Ca2+]i transient. Both effects were absent in the quiescent cell population. The [Ca2+]i transient persisted in low (10 nM) Ca2+ solution and in the presence of 4 mM extracellular Ni2+ but was abolished in the presence of the endoplasmic reticulum Ca2+-ATPase blocker 2,5-di-tert-butyl-hydrochinone (t-BHQ). The t-BHQ likewise inhibited RVD, indicating that Ca2+ release from intracellular stores was necessary for RVD. Moreover, [Ca2+]i and RVD were dependent on an intact microfilament cytoskeleton because after 30 min of preincubation with cytochalasin B the [Ca2+]i transient was significantly reduced and RVD was abolished. The absence of RVD and [Ca2+]i transient in quiescent cells may be due to differences in the amount and the cytosolic arrangement of F-actin observed in quiescent cells.
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PMID:Hypotonic Ca2+ signaling and volume regulation in proliferating and quiescent cells from multicellular spheroids. 952 71

In androgen-responsive LNCaP human prostatic cancer cells, human TR3 orphan receptor, a member of the steroid receptor superfamily, can be rapidly induced by androgen. In contrast, ablation of androgen by castration can induce the expression of the TR3 orphan receptor gene in rat ventral prostate that has undergone apoptosis. This phenomenon prompted us to further analyze the potential role of human TR3 orphan receptor in prostate cancer cells in which apoptosis had been induced. Northern blot analysis shows that human TR3 orphan receptor expression can be induced rapidly after treatment of LNCaP and PC-3 prostate cancer cells with calcium ionophore or etoposide. Our data further demonstrate that a much higher concentration of etoposide was needed to kill the same number of cells in LNCaP and PC-3 cells transfected stably with antisense TR3 orphan receptor compared with that in control vector transfectants. Together, our data suggest that the human TR3 orphan receptor may play an important role in modulating drug-induced prostate apoptosis.
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PMID:Antisense TR3 orphan receptor can increase prostate cancer cell viability with etoposide treatment. 956 41

Osteolytic metastases are often associated with decreased renal tubular reabsorption of phosphate. There is, however, no specific data on phosphate metabolism in metastases from prostatic cancer, which are generally osteoblastic. The aim of the present study was to investigate renal handling of inorganic phosphate (Pi) in prostatic cancer, in patients without or with skeletal metastases of various extents. Forty-eight patients were the subjects of this study. There were 39 with malignant disease, of whom 27 had bony metastases. Nine other patients had benign prostate hyperplasia. Biochemical indexes of prostatic tumor, renal tubular reabsorption of calcium and Pi, biochemical markers of bone remodeling, and relevant calciotropic hormones were measured and analyzed in relation to the extent of skeletal metastases, as assessed by bone scintigraphy. A higher bone metastatic load was associated with significantly greater prostate-specific antigen and prostatic acid phosphatase levels (P < 0.05), increased levels of biochemical markers of bone formation (P < 0.05) and resorption (P < 0.001), higher maximal renal tubular reabsorption of Pi (TmPi/GFR; P < 0.05), and higher urinary cAMP excretion (P < 0.05). Nine patients among those with bone metastases (n = 27) had higher TmPi/GFR than metastasis-free patients. These had a greater value of osteocalcin (P < 0.001). Also, 8 of these had relatively more extensive skeletal metastatic load. In patients with prostatic cancer, high skeletal metastatic load was accompanied by increased TmPi/GFR despite higher urinary cAMP excretion, which is supposed to reduce the TmPi/GFR. These results support the hypothesis that renal tubular reabsorption of Pi is capable of adaptation to meet demands for minerals in the face of enhanced bone formation.
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PMID:Renal tubular reabsorption of phosphate is positively related to the extent of bone metastatic load in patients with prostate cancer. 958 51

The best preventive care consists of a combination of office-based services: patient education, life style counseling, clinical vigilance through routine check ups, and the administration of timely screening. In a healthcare environment of tightened resources, tighter schedules, and increased patient demand for your time, it is nevertheless possible to offer substantive preventive care for older patients in an efficient and cost effective manner. Interventions for cardiovascular disease include weight loss, a low-fat diet, vitamin E, and folic acid. Screening is recommended for breast, cervical, and colon cancer, but prostate cancer screening is controversial. The value of mammograms in women over age 50 is well-established. Preventive measures for osteoporosis include calcium and vitamin D, estrogen replacement, and weight-bearing exercise.
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PMID:Simple, sensible preventive measures for managed care settings. 979 Nov 97

P-Cadherin is a member of the cadherin family of cell surface glycoproteins that mediate Ca2+-dependent cell-cell adhesion and is expressed in a differential fashion in normal epithelial tissues. The expression of P-cadherin in human prostate cancer development has not been investigated previously. By immunohistochemistry, we show that P-cadherin expression is restricted to the cell-cell border of basal epithelial cells in 30 normal prostate samples. This staining is down-regulated in prostatic intraepithelial neoplasia and is absent in all 25 of the well to poorly differentiated prostate cancer specimens analyzed. To examine potential P-cadherin-regulatory elements, we sequenced the 5'-flanking region of this gene. Similar to the mouse gene, the human P-cadherin promoter is TATA-less, contains an Sp-1 binding site and, analogous to the human E-cadherin sequence, demonstrates a GC-rich region characteristic of a CpG island. Cytosine methylation of this region occurs in P-cadherin-negative prostate cancer cell lines but not in cell lines expressing this gene. In vivo, a lack of expression in 12 clinical prostate cancer specimens is not associated with methylation of the P-cadherin promoter. These results demonstrate that the expression of the basal cell marker P-cadherin is lost in prostate cancer development and that in vivo mechanisms other than cytosine methylation regulate this consistent loss of expression.
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PMID:P-Cadherin is a basal cell-specific epithelial marker that is not expressed in prostate cancer. 981 5


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