Search results for: Prostatic Acid Phosphatase
#29260582 // Save this To Up
Sipuleucel-T for the treatment of prostate cancer: novel insights and future directions.Sipuleucel-T, an autologous cellular immunotherapy manufactured from antigen-presenting cells primed to recognize prostatic acid phosphatase, was the first immunotherapy product approved by the US FDA. It was approved for men with asymptomatic or minimally symptomatic metastatic castration-resistant prostate cancer after it was shown to provide a survival advantage. Additional studies have examined its use in other clinical settings and in combination with other approved and investigational immunotherapy agents. This review will discuss the pivotal trials leading to approval, will outline some of the biomarkers associated with its efficacy and will review some of the ongoing combination strategies. Maximizing the efficacy of sipuleucel-T through better patient selection or through combination approaches remains the challenge of the future.
1782 related Products with: Sipuleucel-T for the treatment of prostate cancer: novel insights and future directions.Prostate cancer and hyper Prostate cancer, adjacent Multiple organ cancer tis Prostate cancer tissue ar High density prostate can High density (70 cases 20 High density (114 cases 2 High density (208 core) p Prostate cancer test tiss Multiple prostate cancer Prostate cancer tissue ar Prostate cancer and norma
#29134981 // Save this To Up
Biochemical, Hormonal and Histological Changes in Prostate of Wistar Rats Following Long Term Streptozotocin-induced Diabetes Mellitus.Diabetes mellitus (DM) is characterized by hyperglycemia and endocrine disorder. Diabetes mellitus is knownto promote male infertility by affecting sperm quality through altered steroidogenesis. The role of prostatic fluid in maintenance of sperm quality have been established. However, the effect of DM on prostate health is poorly understood.This study was designed to investigate the biochemical, hormonal and histological changes in prostate of male Wistar ratsafter 3- and 5-months DM. Twenty-six adult male Wistar rats were assigned into three groups. Group I (non-diabetic rats)served as control (n=10), out of which five rats (n=5) were sacrificed as control for 3-month study and the remaining animals(n=5) as control for 5-month study. Group II served as 3-month DM (n=8) and group III served as 5-month DM (n=8).Diabetes mellitus was induced by administration of a single dose of streptozotocin (STZ) (35 mg/kg i.p.). Rats were sacrificedat 3- and 5- months after DM. Biochemical indices in serum and prostate, histological and immunohistochemical studies ofthe prostate were evaluated. Results indicated that the weight of prostate of 3- and 5-months DM rats significantly (p<0.05)decreased by 33% and 59%, respectively. Fasting blood glucose, plasma glycated haemoglobin and number ofmicronucleated polychromatic erythrocytes in the bone marrow significantly (p<0.05) increased in 3- and 5-months DM.Activities of serum alanine and aspartate aminotransferases significantly (p<0.05) increased in 3 months DM withconcomitant increase in serum total bilirubin and urea in both models. The activities of total acid phosphatase in 3- and 5-months DM decreased by 34% and 76%, respectively while prostatic acid phosphatase decreased by 48% in 5-months DM.Prostatic zinc and bicarbonate increased in 3-months DM by 1.7 and 1.9 folds, and in 5-months DM by 5.8 and 1.7 folds,respectively. The levels of serum luteinizing and follicle stimulating hormones and testosterone decreased in both models.Prostatic lipid peroxidation increased while activities of antioxidative enzymes decreased in both models. Histology revealedhyperplasia, intra-luminal budding of epithelia, mild expressions of Bcl2 and Ki67 in 3- and 5-months DM. Overall, prostate health was compromised and may increase infertility in diabetic animals.
2610 related Products with: Biochemical, Hormonal and Histological Changes in Prostate of Wistar Rats Following Long Term Streptozotocin-induced Diabetes Mellitus.Interleukin-34 IL34 (N-t Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Human Epstein-Barr Virus Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Goat Anti-Human HMGB3 HMG Goat Anti-Human F2R PAR1,
#28844848 // Save this To Up
Nano-sized titanium dioxide toxicity in rat prostate and testis: Possible ameliorative effect of morin.This study investigated the effect of short-term oral exposure to nano-sized titanium dioxide (nTiO) on Wistar rat prostate and testis, and the associating reproductive-related alterations. The study also evaluated the potential ameliorative effect of the natural flavonoid, morin, on nTiO-induced aberrations. Intragastric administration of nTiO(50mg/kg/day for 1, 2 and 3weeks) increased testicular gamma-glutamyltransferase (γ-GT) activity and decreased testicular steroidogenic acute regulatory protein (StAR) and c-kit gene expression, serum testosterone level and sperm count. nTiO-treated rats also exhibited prostatic and testicular altered glutathione levels, elevated TNF-α levels, up-regulated Fas, Bax and caspase-3 gene expression, down-regulated Bcl-2 gene expression and enhanced prostatic lipid peroxidation. Sperm malformation and elevated testicular acid phosphatase (ACP) activity and malondialdehyde level, serum prostatic acid phosphatase activity, prostate specific antigen (PSA), gonadotrophin and estradiol levels occurred after the 2 and 3week regimens. Morin (30mg/kg/day administered intragastrically for 5weeks) mitigated nTiO-induced prostatic and testicular injury as evidenced by lowering serum PSA level, testicular γ-GT and ACP activities and TNF-α level, along with hampering both intrinsic and extrinsic apoptotic pathways. Moreover, morin alleviated prostatic lipid peroxidation, raised prostatic glutathione level, and relieved testicular reductive stress. Additionally, morin increased testicular StAR and c-kit mRNA expression, raised the sperm count, reduced sperm deformities and modified the altered hormone profile. Histopathological evaluation supported the biochemical findings. In conclusion, morin could ameliorate nTiO-induced prostatic and testicular injury and the corresponding reproductive-related aberrations via redox regulatory, anti-inflammatory and anti-apoptotic mechanisms, promoting steroidogenesis and spermatogenesis, and improving sperm count and morphology.
2750 related Products with: Nano-sized titanium dioxide toxicity in rat prostate and testis: Possible ameliorative effect of morin.Sterile filtered rat ser Insulin 1 (Rat), syntheti Goat Anti-Rat MARCH10, (i Goat Anti-Mouse, Rat DLL1 Goat Anti-Human, Mouse, R Goat Anti-Human, Mouse, R Goat Anti-Rat Connexin 43 Goat Anti-Human, Rat CHRN Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki
#28716080 // Save this To Up
Pretreatment antigen-specific immunity and regulation - association with subsequent immune response to anti-tumor DNA vaccination.Immunotherapies have demonstrated clinical benefit for many types of cancers, however many patients do not respond, and treatment-related adverse effects can be severe. Hence many efforts are underway to identify treatment predictive biomarkers. We have reported the results of two phase I trials using a DNA vaccine encoding prostatic acid phosphatase (PAP) in patients with biochemically recurrent prostate cancer. In both trials, persistent PAP-specific Th1 immunity developed in some patients, and this was associated with favorable changes in serum PSA kinetics. In the current study, we sought to determine if measures of antigen-specific or antigen non-specific immunity were present prior to treatment, and associated with subsequent immune response, to identify possible predictive immune biomarkers.
1762 related Products with: Pretreatment antigen-specific immunity and regulation - association with subsequent immune response to anti-tumor DNA vaccination.MOUSE ANTI BORRELIA BURGD Mouse Anti-Prostate Speci Mouse Anti-Rotovirus Grou FDA normal and tumor orga FDA normal and tumor orga FDA normal and tumor orga Rabbit Anti-Clostridium b Mouse Anti-Rotavirus Grou Prostate cancer, hyperpla PSA (Prostate Specific A PSA (Prostate Specific A PSA (Prostate Specific A
#28621316 // Save this To Up
Combination of p53-DC vaccine and rAd-p53 gene therapy induced CTLs cytotoxic against p53-deleted human prostate cancer cells in vitro.Recently, the US FDA approved sipuleucel-T, which is composed of autologous DCs stimulated with a recombinant fusion protein of prostatic acid phosphatase (PAP) and granulocyte-macrophage colony-stimulating factor (GM-CSF), as the first immunotherapeutic agent for metastatic castration resistant prostate cancer (mCRPC). However, sipuleucel-T demonstrated only modest efficacy in mCPRC patients. Researchers are now investigating the potential of p53 protein as a tumor-associated antigen (TAA) loaded in DC-based cancer vaccine. Approximately half of all tumors overexpress p53, and up to 20% of prostate cancer cells overexpresses p53. In this study, we evaluated the feasibility of combining p53-DC vaccine and rAd-p53 gene therapy, using the p53-overexpressing and non-expressing prostate cancer cells in vitro. We successfully generated the p53-DC vaccine by culturing autologous DCs infected with rAd-p53. This p53-DC vaccine can differentiate CTLs specifically cytotoxic to p53-overexpressing prostate cancer cells. In addition, rAd-p53 infection can induce overexpression of p53 and thus the cytotoxicity of CTLs differentiated by the p53-DC vaccine in p53 non-expressing prostate cancer cells. These findings suggest that this combination therapy using p53-DC vaccine and rAd-p53 gene therapy together may represent a new paradigm for the treatment of mCRPC.
2599 related Products with: Combination of p53-DC vaccine and rAd-p53 gene therapy induced CTLs cytotoxic against p53-deleted human prostate cancer cells in vitro.Breast cancer tissue arra Breast cancer tissue arra Human Epstein-Barr Virus Mouse Anti-Human p53 Anti Mouse Anti-Human p53 Anti Mouse Anti-Human P53 Anti Mouse Anti-Human P53 Anti Recombinant Human p53 Mut Recombinant Human p53 Mut Recombinant Human p53 Mut p53, human recombinant p53 Mutant, human recombi
#28555048 // Save this To Up
Sensitivity of HOXB13 as a Diagnostic Immunohistochemical Marker of Prostatic Origin in Prostate Cancer Metastases: Comparison to PSA, Prostein, Androgen Receptor, ERG, NKX3.1, PSAP, and PSMA.Determining the origin of metastases is an important task of pathologists to allow for the initiation of a tumor-specific therapy. Recently, homeobox protein Hox-B13 (HOXB13) has been suggested as a new marker for the detection of prostatic origin. The aim of this study was to evaluate the diagnostic sensitivity of HOXB13 in comparison to commonly used immunohistochemical markers for prostate cancer.
1585 related Products with: Sensitivity of HOXB13 as a Diagnostic Immunohistochemical Marker of Prostatic Origin in Prostate Cancer Metastases: Comparison to PSA, Prostein, Androgen Receptor, ERG, NKX3.1, PSAP, and PSMA.Prostate cancer, PIN (pro Prostate cancer, hyperpla Top 4 types of cancer (co Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 Cell Meter™ Fluorimetri Cell Meter™ Fluorimetri AZD-3514 Mechanisms: Andr Top five cancer tissue ar
#28461585 // Save this To Up
Up-regulated Ectonucleotidases in Fas-Associated Death Domain Protein- and Receptor-Interacting Protein Kinase 1-Deficient Jurkat Leukemia Cells Counteract Extracellular ATP/AMP Accumulation via Pannexin-1 Channels during Chemotherapeutic Drug-Induced Apoptosis.Pannexin-1 (Panx1) channels mediate the efflux of ATP and AMP from cancer cells in response to induction of extrinsic apoptosis by death receptors or intrinsic apoptosis by chemotherapeutic agents. We previously described the accumulation of extracellular ATP /AMP during chemotherapy-induced apoptosis in Jurkat human leukemia cells. In this study, we compared how different signaling pathways determine extracellular nucleotide pools in control Jurkat cells versus Jurkat lines that lack the Fas-associated death domain (FADD) or receptor-interacting protein kinase 1 (RIP1) cell death regulatory proteins. Tumor necrosis factor-induced extrinsic apoptosis in control Jurkat cells and necroptosis in FADD-deficient cells; treatment of both lines with chemotherapeutic drugs elicited similar intrinsic apoptosis. Robust extracellular ATP/AMP accumulation was observed in the FADD-deficient cells during necroptosis, but not during apoptotic activation of Panx1 channels. Accumulation of extracellular ATP/AMP was similarly absent in RIP1-deficient Jurkat cells during apoptotic responses to chemotherapeutic agents. Apoptotic activation triggered equivalent proteolytic gating of Panx1 channels in all three Jurkat cell lines. The differences in extracellular ATP/AMP accumulation correlated with cell-line-specific expression of ectonucleotidases that metabolized the released ATP/AMP. CD73 mRNA, and-methylene-ADP-inhibitable ecto-AMPase activity were elevated in the FADD-deficient cells. In contrast, the RIP1-deficient cells were defined by increased expression of tartrate-sensitive prostatic acid phosphatase as a broadly acting ectonucleotidase. Thus, extracellular nucleotide accumulation during regulated tumor cell death involves interplay between ATP/AMP efflux pathways and different cell-autonomous ectonucleotidases. Differential expression of particular ectonucleotidases in tumor cell variants will determine whether chemotherapy-induced activation of Panx1 channels drives accumulation of immunostimulatory ATP versus immunosuppressive adenosine within the tumor microenvironment.
2427 related Products with: Up-regulated Ectonucleotidases in Fas-Associated Death Domain Protein- and Receptor-Interacting Protein Kinase 1-Deficient Jurkat Leukemia Cells Counteract Extracellular ATP/AMP Accumulation via Pannexin-1 Channels during Chemotherapeutic Drug-Induced Apoptosis.Polyclonal Antibody Recep anti FAS IgG1 (monoclonal MID1 interacting G12-like Rabbit Anti-APIP Apaf1 In Rabbit Anti-APIP Apaf1 In Rabbit Anti-APIP Apaf1 In Rabbit Anti-APIP Apaf1 In Rabbit Anti-APIP Apaf1 In Rabbit Anti-APIP Apaf1 In Rabbit Anti-APIP Apaf1 In Rabbit Anti-APIP Apaf1 In Rabbit Anti-APIP Apaf1 In
#28416373 // Save this To Up
Inhibition effects of chlorogenic acid on benign prostatic hyperplasia in mice.This study aimed to evaluate the inhibitory effects and explore mechanisms of chlorogenic acid against testosterone-induced benign prostatic hyperplasia (BPH) in mice. Benign prostatic hyperplasia model was induced in experimental groups by daily subcutaneous injections of testosterone propionate (7.5mg/kg/d) consecutively for 14 d. A total of 60 mice were randomly divided into six groups: (Group 1) normal control group, (Group 2) benign prostatic hyperplasia model control group, (Group 3) benign prostatic hyperplasia mice treated with finasteride at a dose of 1mg/kg, (Group 4) benign prostatic hyperplasia mice treated with chlorogenic acid at dose levels of 0.8mg/kg (low dose group), (Group 5) benign prostatic hyperplasia mice treated with chlorogenic acid at dose levels of 1.6mg/kg (medium dose group) and (Group 6) benign prostatic hyperplasia mice treated with chlorogenic acid at dose levels of 3.2mg/kg (high dose group). Animals were sacrificed on the scheduled termination, pick out the eyeball to get blood, then prostates were weighed and prostatic index were determined. Then the serum acid phosphatase (ACP), prostatic acid phosphatase (PACP) and typeⅡ5-alpha-reductase (SRD5A2) levels were measured and observed morphological changes of the prostate. Comparing with benign prostatic hyperplasia model group, the high and medium dose of chlorogenic acid could significantly reduce prostate index and levels of acid phosphatase, prostatic acid phosphatase and typeⅡ5-alpha-reductase (P<0.05 or P<0.01). These findings were supported by histopathological observations of prostate tissues. Histopathological examination also indicated that chlorogenic acid treatment at the high and medium doses inhibited testosterone-induced prostatic hyperplasia. The results indicated that chlorogenic acid exhibited restraining effect on benign prostatic hyperplasia model animals, and its mechanism might be related to inhibit typeⅡ5-alpha reductase activity.
2197 related Products with: Inhibition effects of chlorogenic acid on benign prostatic hyperplasia in mice.Prostate cancer, PIN (pro Anti-Human Benign Prostat Anti-Human Benign Prostat GST Inhibitor 2 (Ethacryn Directed In Vivo Angiogen α-Acetamino-α-carboxy-( N-Acetyl-2-O-(5-bromo-1H- (1R,3S)-1-(1,3-Benzodioxo (1S,3S)-1-(1,3-Benzodioxo (1S,3S)-1-(1,3-Benzodioxo (1R,3S)-1-(1,3-Benzodioxo Rabbit Anti-IAA (Indole-3
#28376158 // Save this To Up
Role of Antigen Spread and Distinctive Characteristics of Immunotherapy in Cancer Treatment.Immunotherapy is an important breakthrough in cancer. US Food and Drug Administration-approved immunotherapies for cancer treatment (including, but not limited to, sipuleucel-T, ipilimumab, nivolumab, pembrolizumab, and atezolizumab) substantially improve overall survival across multiple malignancies. One mechanism of action of these treatments is to induce an immune response against antigen-bearing tumor cells; the resultant cell death releases secondary (nontargeted) tumor antigens. Secondary antigens prime subsequent immune responses (antigen spread). Immunotherapy-induced antigen spread has been shown in clinical studies. For example, in metastatic castration-resistant prostate cancer patients, sipuleucel-T induced early immune responses to the immunizing antigen (PA2024) and/or the target antigen (prostatic acid phosphatase). Thereafter, most patients developed increased antibody responses to numerous secondary proteins, several of which are expressed in prostate cancer with functional relevance in cancer. The ipilimumab-induced antibody profile in melanoma patients shows that antigen spread also occurs with immune checkpoint blockade. In contrast to chemotherapy, immunotherapy often does not result in short-term changes in conventional disease progression end points (eg, progression-free survival, tumor size), which may be explained, in part, by the time taken for antigen spread to occur. Thus, immune-related response criteria need to be identified to better monitor the effectiveness of immunotherapy. As immunotherapy antitumor effects take time to evolve, immunotherapy in patients with less advanced cancer may have greater clinical benefit vs those with more advanced disease. This concept is supported by prostate cancer clinical studies with sipuleucel-T, PSA-TRICOM, and ipilimumab. We discuss antigen spread with cancer immunotherapy and its implications for clinical outcomes.
1687 related Products with: Role of Antigen Spread and Distinctive Characteristics of Immunotherapy in Cancer Treatment.Prostate cancer, hyperpla CA125, Ovarian Cancer An CA125, Ovarian Cancer An CA125, Ovarian Cancer An HIV 1 intergase antigen. anti H inh human blood an H. Pylori antigen test ca Malaria pan antigen test, Malaria pf antigen test, Malaria pf pv antigen tes serologically defined col Anti beta3 AR Human, Poly
#28361045 // Save this To Up
Phase I clinical trial of sipuleucel-T combined with escalating doses of ipilimumab in progressive metastatic castrate-resistant prostate cancer.Sipuleucel-T (SIP-T), which functions by stimulating cancer-specific dendritic cells, prolongs survival in men with prostate cancer. Ipilimumab (IPI) achieved a borderline survival advantage in a large randomized trial. SIP-T and IPI are potentially synergistic.
2412 related Products with: Phase I clinical trial of sipuleucel-T combined with escalating doses of ipilimumab in progressive metastatic castrate-resistant prostate cancer.Prostate cancer, adjacent Breast cancer and matched Lung cancer tissue array Prostate cancer tissue ar Prostate cancer tissue ar Prostate cancer tissue ar Prostate cancer tissue ar Prostate cancer tissue ar Prostate cancer tissue ar Prostate cancer test tiss Prostate cancer test tiss Prostate cancer test tiss
Voortstraat 49, 1910 Kampenhout BELGIUM
Tel 0032 16 58 90 45 Fax 0032 16 50 90 45
9, rue Lagrange, 75005 Paris
Tel 01 43 25 01 50 Fax 01 43 25 01 60
52062 Aachen Deutschland
Tel 0241 40 08 90 86 Fax 0241 55 91 05 36
Howard Frank Turnberry House
1404-1410 High Road
Whetstone London N20 9BH
Tel 020 3393 8531 Fax 020 8445 9411
Schweiz Züri +41435006251
Česká republika Praha +420246019719
Ireland Dublin +35316526556
Norge Oslo +4721031366
Finland Helsset +358942419041
Sverige Stockholm +46852503438
Ελλάς Αθήνα +302111768494
Magyarország Budapest +3619980547
GENTAUR Poland Sp. z o.o.
ul. Grunwaldzka 88/A m.2
81-771 Sopot, Poland
Tel 058 710 33 44
Fax 058 710 33 48
GENTAUR Nederland BV
5521 DG Eersel Nederland
Tel 0208-080893 Fax 0497-517897
Piazza Giacomo Matteotti, 6, 24122 Bergamo
Tel 02 36 00 65 93 Fax 02 36 00 65 94
53 Iskar Str. 1191 Kokalyane, Sofia