Radium 223 combined with new hormone therapies for the treatment of castrate-resistant metastatic prostate cancer: scientific evidence and sharing of our experience.

Potent repression of C-reactive protein (CRP) expression by the JAK1/2 inhibitor ruxolitinib in inflammatory human hepatocytes

by
To determine whether inflammatory hepatocytes may constitute primary targets for ruxolitinib, a Janus kinase (JAK) inhibitor, its effects towards expression of hepatic acute-phase proteins, especially C-reactive protein (CRP), were assessed.Ruxolitinib effects were analysed in primary human hepatocytes and human hepatoma HepaRG cells exposed to various inflammatory stimuli.
RESULTS

Ruxolitinib was found to fully inhibit lipopolysaccharide (LPS)-induced CRP secretion and mRNA expression, at concentrations (IC50 = 12.9 nM) achievable in human blood. It similarly repressed CRP up-regulation due to several Toll-like receptor agonists or pro-inflammatory cytokines [interleukin (IL) 1β, IL6 and tumour necrosis factor α] and counteracted LPS-mediated induction of serum amyloid A, fibrinogen, haptoglobin and serpin. Ruxolitinib was additionally found to block the activation of the IL6/JAK/signal transducer and activator of transcription (STAT) pathway triggered by LPS and whose inhibition by the neutralizing anti-IL6 receptor antibody tocilizumab prevented CRP induction.Ruxolitinib can potently repress induction of CRP in inflammatory human hepatocytes, most likely through targeting the IL6/JAK/STAT signalling cascade. Hepatic production of acute-phase proteins during liver inflammation may, therefore, constitute a target for ruxolitinib.

Nanomolar aluminum induces expression of the inflammatory systemic biomarker C–reactive protein (CRP) in human brain microvessel endothelial cells (hBMECs).

C-reactive protein (CRP; also known as pentraxin 1, PTX1), a 224 amino acid soluble serum protein organized into a novel pentameric ring-shaped structure, is a highly sensitive pathogenic biomarker for systemic inflammation. High CRP levels are found in practically every known inflammatory state, and elevated CRP levels indicate an increased risk for several common age-related human degenerative disorders, including cardiovascular disease, cancer, diabetes, and Alzheimer’s disease (AD). While the majority of CRP is synthesized in the liver for secretion into the systemic circulation, it has recently been discovered that an appreciable amount of CRP is synthesized in highly specialized endothelial cells that line the vasculature of the brain and central nervous system (CNS).
These highly specialized cells, the major cell type lining the human CNS vasculature, are known as human brain microvessel endothelial cells (hBMECs). In the current pilot study we examined (i) CRP levels in human serum obtained from AD and age-matched control patients; and (ii) analyzed the effects of nanomolar aluminum sulfate on CRP expression in primary hBMECs. The three major findings in this short communication are: (i) that CRP is up-regulated in AD serum; (ii) that CRP serum levels increased in parallel with AD progression; and (iii) for the first time show that nanomolar aluminum potently up-regulates CRP expression in hBMECs to many times its ‘basal abundance’. The results suggest that aluminum-induced CRP may in part contribute to a pathophysiological state associated with a chronic systemic inflammation of the human vasculature.

High sensitivity C–reactive protein (Hs-CRP) remains highly stable in long-term archived human serum.

BACKGROUND
The stability of biomarkers in stored biomedical samples is crucial, especially when storage is for extended periods of time. High-sensitivity CRP (Hs-CRP) is a biomarker of low grade inflammation that is extensively used to identify and study cardiovascular and/or inflammatory processes in clinical care and large epidemiologic studies. Therefore, assessing Hs-CRP stability in archived samples at a given temperature is important to ensure precision of measurements over time and the validity of studies using archived samples.
METHODS
We evaluated the stability of Hs-CRP in 30 randomly selected human serum samples by measuring Hs-CRP concentrations in freshly collected sample [Hs-CRP (0)] and in the same set of samples after 7-11years of storage at -80°C [Hs-CRP (LT)].
RESULTS
Hs-CRP did not significantly change up to 11years of storage at -80°C as shown by a negligible median difference between Hs-CRP (0) and Hs-CRP (LT), delta(Hs-CRP (0)-Hs-CRP (LT))=-0.01, p=0.45. There was a good concordance and agreement between Hs-CRP (0) and Hs-CRP (LT) as measured respectively by Lin’s coefficient of correlation (ρC=0.98) and Bland-Altman analysis (mean difference=-0.02, 95% CI [-0.04-0.0045] p=0.107). In addition, the data also suggest that the time elapsed between collection and Hs-CRP measurement does not affect Hs-CRP stability over time when samples are kept under the appropriate conditions.
CONCLUSIONS
Long-term storage at -80°C for up to 11years did not significantly affect the stability of serum Hs-CRP. Given the cost and time for collecting fresh samples, this observation represents an important finding for biomedical research and clinical care.

C–reactive protein (CRP) induces chemokine secretion via CD11b/ICAM-1 interaction in human adherent monocytes.

Several studies support C-reactive protein (CRP) as a systemic cardiovascular risk factor. The recent detection of CRP in arterial intima suggests a dual activity in atherosclerosis as a circulating and tissue mediator on vascular and immune cells. In the present paper, we focused on the inflammatory effects of CRP on human monocytes, which were isolated by Ficoll-Percoll gradients and cultured in adherence to polystyrene, endothelial cell monolayer, or in suspension. Chemokine levels, adhesion molecule, and chemokine receptor expression were detected by ELISA, flow cytometry, and real-time RT-PCR. Migration assays were performed in a Boyden chamber. Stimulation with CRP induced release of CCL2, CCL3, and CCL4 in adherent monocytes through the binding to CD32a, CD32b, and CD64, whereas no effect was observed in suspension culture.
This was associated with CRP-induced up-regulation of adhesion molecules membrane-activated complex 1 (Mac-1) and ICAM-1 on adherent monocytes. Blockade of Mac-1/ICAM-1 interaction inhibited the CRP-induced chemokine secretion. In addition, CRP reduced mRNA and surface expression of corresponding chemokine receptors CCR1, CCR2, and CCR5 in adherent monocytes. This effect was a result of chemokine secretion, as coincubation with neutralizing anti-CCL2, anti-CCL3, and anti-CCL4 antibodies reversed the effect of CRP. Accordingly, a reduced migration of CRP-treated monocytes to CCL2 and CCL3 was observed. In conclusion, our data suggest an in vitro model to study CRP activities in adherent and suspension human monocytes. CRP-mediated induction of adhesion molecules and a decrease of chemokine receptors on adherent monocytes might contribute to the retention of monocytes within atherosclerotic lesions and recruitment of other circulating cells.

Human C Reactive Protein (CRP) Protein
20-abx168571 Abbexa
  • Ask for price
  • Ask for price
  • Ask for price
  • Ask for price
  • Ask for price
  • 10 ug
  • 50 ug
  • 100 ug
  • 200 ug
  • 1 mg

Human C Reactive Protein (CRP) Protein
abx168571-1ml Abbexa 1 ml 175 EUR

Human C Reactive Protein (CRP) Protein
abx065612-100g Abbexa 100 µg 325 EUR

Human C Reactive Protein (CRP) Protein
20-abx065612 Abbexa
  • Ask for price
  • Ask for price
  • Ask for price
  • Ask for price
  • Ask for price
  • 10 ug
  • 50 ug
  • 100 ug
  • 200 ug
  • 1 mg

Human C Reactive Protein (CRP) Protein
abx065612-10g Abbexa 10 µg 162.5 EUR

Human C Reactive Protein (CRP) Protein
abx065612-50g Abbexa 50 µg 250 EUR

C Reactive Protein (CRP)
MBS319534-1mg MyBiosource 1mg 505 EUR

C Reactive Protein (CRP)
MBS319534-5x1mg MyBiosource 5x1mg 2100 EUR

C Reactive Protein (CRP)
MBS319547-1mg MyBiosource 1mg 1230 EUR

C Reactive Protein (CRP)
MBS319547-5x1mg MyBiosource 5x1mg 5360 EUR

C Reactive Protein (CRP)
MBS590047-192Wells MyBiosource 192Wells 995 EUR

C Reactive Protein (CRP)
MBS590047-3x192Wells MyBiosource 3x192Wells 2195 EUR

C Reactive Protein (CRP)
MBS590047-96Wells MyBiosource 96Wells 675 EUR

C Reactive Protein (CRP)
THP-0256 Creative BioMart 10mg 3198.4 EUR

Human C Reactive Protein (CRP) CLIA Kit
20-abx490698 Abbexa
  • Ask for price
  • Ask for price
  • Ask for price
  • 96 tests
  • 5 × 96 tests
  • 10 × 96 tests

Human C Reactive Protein (CRP) CLIA Kit
EKN50029-48T Biomatik Corporation 48T 414.89 EUR

Human C Reactive Protein (CRP) CLIA Kit
EKN50029-5x96T Biomatik Corporation 5x96T 2815.33 EUR

Human C Reactive Protein (CRP) CLIA Kit
EKN50029-96T Biomatik Corporation 96T 592.7 EUR

Human C Reactive Protein (CRP) CLIA Kit
EKU08918-48T Biomatik Corporation 48T 666.82 EUR

Human C Reactive Protein (CRP) CLIA Kit
EKU08918-5x96T Biomatik Corporation 5x96T 4524.85 EUR

Human C Reactive Protein (CRP) CLIA Kit
EKU08918-96T Biomatik Corporation 96T 952.6 EUR

Human C Reactive Protein (CRP) CLIA Kit
MBS2708864-10x96StripWells MyBiosource 10x96-Strip-Wells 3735 EUR

Human C Reactive Protein (CRP) CLIA Kit
MBS2708864-24StripWells MyBiosource 24-Strip-Wells 275 EUR

Human C Reactive Protein (CRP) CLIA Kit
MBS2708864-48StripWells MyBiosource 48-Strip-Wells 365 EUR

Human C Reactive Protein (CRP) CLIA Kit
MBS2708864-5x96StripWells MyBiosource 5x96-Strip-Wells 1935 EUR

Human C Reactive Protein (CRP) CLIA Kit
MBS2708864-96StripWells MyBiosource 96-Strip-Wells 480 EUR

Polymorphism in the human C–reactive protein (CRP) gene, serum concentrations of CRP, and the difference between intracranial and extracranial atherosclerosis.

BACKGROUND
C-reactive protein, a proinflammatory factor, is involved in the development of atherosclerosis. The CRP 1059G>C polymorphism appeared to be a susceptive marker for atherosclerosis. We investigated the relationship of the distribution of cerebral atherosclerosis with triggered serum CRP concentrations following acute ischemic stroke/transient ischemic attack (IS/TIA) and CRP 1059G>C polymorphism.
METHODS
We recruited 222 IS/TIA patients (122 with only intracranial atherosclerotic lesions and 100 with isolated extracranial atherosclerotic lesions) and 227 controls. Intra- and extracranial atherosclerotic lesions were determined by digital subtraction angiography. Serum CRP concentrations were measured by particle-enhanced immunonephelometry assay. CRP 1059G>C genotypes were obtained through PCR amplification and restriction enzyme digestion.
RESULTS
CRP concentrations were significantly higher in intra- and extracranial groups than in controls. No significant difference was found in CRP concentrations between intra- and extracranial groups. The CRP 1059G>C single-nucleotide polymorphism did not influence CRP serum concentrations. CRP genotype and allele frequencies did not differ significantly between patients and controls. However, the frequencies of GC genotype and C allele were significantly higher in extracranial group than that in intracranial group. The GC individuals showed a higher risk of extracranial atherosclerosis compared with GG individuals (OR 3.41; 95%CI, 1.124-10.347; P=0.030).
CONCLUSIONS
Serum CRP is associated with cerebral atherosclerotic disease. CRP 1059G>C polymorphism is one possible genetic determinant for the difference between intra- and extracranial atherosclerosis.

Comparison and commutability study between standardized liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS) and chemiluminescent enzyme immunoassay for aldosterone measurement in blood

by
A commutability confirmation test for the blood aldosterone measurement was performed on liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS) as a designated comparison method (DCM) and four chemiluminescent enzyme immunoassay (CLEIA) measurement procedures based on metrological traceability. A conventional radioimmunoassay (RIA) and two measurement procedures of CLEIA which obtains RIA equivalent values were also compared. The relationship between the DCM value and the CLEIA value with respect to 120 pg/mL of the RIA value, which is the screening criterion of primary aldosteronism (PA) was clarified. For the correlation test, 75 samples of patient serum and plasma were used. Regression analysis revealed that the standardized LC-MS/MS and four CLEIA measurement procedures were in good agreement.
This is the effect of measurement specificity and calibration using by certified reference material (CRM). The median of the LC-MS/MS corresponding to 120 pg/mL of RIA was 48.5 pg/mL. In the mean of standardized four CLEIA values corresponding to the 48.5 pg/mL of LC-MS/MS value was 47.51 pg/mL and the standard deviation (SD) was 2.93 pg/mL. However, the correlation between the RIA value and the RIA equivalent of the two measurement procedures by CLEIA differed depending on the measurement procedure. This is due to the influence of RIA measurement performance. Standardized CLEIA measurements are suitable for routine measurement procedure. When converting the LC-MS/MS equivalent value by the standardized CLEIA to the conventional RIA value, it is necessary to use the conversion formula.

Comparisons of plasma aldosterone and renin data between an automated chemiluminescent immunoanalyzer and conventional radioimmunoassays in the screening and diagnosis of primary aldosteronism

Determining values of plasma renin activity (PRA) or plasma active renin concentration (ARC), plasma aldosterone concentration (PAC), and aldosterone-to-renin ratio (ARR) is essential to diagnose primary aldosteronism (PA), but it takes several days with conventional radioimmunoassays (RIAs). Chemiluminescent enzyme immunoassays for PAC and ARC using the Accuraseed® immunoanalyzer facilitated the determination, but relations between Accuraseed® immunoanalyzer-based and RIA-based values in samples of PA confirmatory tests and adrenal venous sampling remained to be elucidated. We addressed this issue in the present study. This is a prospective, cross-sectional study. ARC and PAC values were measured by the Accuraseed® immunoanalyzer in samples, in which PRA and PAC values had been measured by the PRA-FR® RIA and SPAC®-S Aldosterone kits, respectively. The relations between Accuraseed® immunoanalyzer-based and RIA-based values were investigated with regression analyses. The optimal cutoff of Accuraseed® immunoanalyzer-based ARR for PA screening was determined by the receiver operating characteristic analysis.
After log-log transformations, linear relations with high coefficients of determination were observed between Accuraseed® immunoanalyzer-based and RIA-based data of renin and aldosterone. Following the PA guidelines of Japan Endocrine Society, Accuraseed® immunoanalyzer-based cutoffs were calculated from the regression equations: the basal PAC for PA screening >12 ng/dL, PAC for the saline infusion test >8.2 ng/dL, ARC for the furosemide-upright test <15 pg/mL, and ARR for the captopril challenge test >3.09 ng/dL per pg/mL. The optimal cutoff of Accuraseed® immunoanalyzer-based ARR for PA screening was >2.43 ng/dL over pg/mL not to overlook bilateral PA patients. The present study provided conversion formulas between Accuraseed® immunoanalyzer-based and RIA-based values of renin, aldosterone, and ARR, not only in basal samples but also in samples of PA confirmatory tests and adrenal venous sampling. Although validation studies are awaited, the present study will become priming water of harmonization of renin and aldosterone immunoassays.

Novel chemiluminescent immunoassay to measure plasma aldosterone and plasma active renin concentrations for the diagnosis of primary aldosteronism

  • Determination of plasma aldosterone concentrations (PAC) and plasma active renin concentrations (ARC) is essential for the diagnosis of primary aldosteronism (PA). In Japan, although PAC and ARC are measured by radioimmunoassay and immunoradiometric assay, respectively, non-radioisotopic methods with better detection sensitivity, measurement accuracy, and technical simplicity are needed. We developed two-site sandwich chemiluminescent enzyme immunoassays (CLEIAs) to measure both PAC and ARC using monoclonal antibodies immobilized onto ferrite particles. The results of both assays are obtained simultaneously from a single plasma sample within 30 min using a fully automated system.
  • The novel CLEIAs were validated using plasma samples from patients with PA (n = 52) and essential hypertension (n = 23). The PAC determined by the CLEIA was significantly correlated with that measured by liquid chromatography/mass spectrometry or conventional radioimmunoassay. The ARC determined by the CLEIA was significantly correlated with that measured by immunoradiometric assay. The limits of detection of the CLEIAs for PAC and ARC were 0.1 ng/dl and 0.04 pg/ml, respectively, which were better than those of conventional methods (PAC: 2.5 ng/dl; ARC: 5 pg/ml).
  • The PAC and PAC/ARC ratio (ARR) were significantly higher, and the ARC significantly lower, in patients with PA than in those with essential hypertension. An ARR cut-off of 1.31 ng/dl per pg/ml showed a sensitivity of 96.2% and specificity of 78.3% for PA screening. The newly developed CLEIAs for measuring PAC and ARC could provide a clinically powerful alternative to conventional methods used for hypertension screening in clinical practice.

Feasibility of Screening Primary Aldosteronism by Aldosterone-to-Direct Renin Concentration Ratio Derived from Chemiluminescent Immunoassay Measurement: Diagnostic Accuracy and Cutoff Value.

<AbstractText>Aldosterone-to-plasma renin activity ratio (ARR) derived from traditional radioimmunoassay (RIA) is widely used to detect primary aldosteronism (PA). Recently, aldosterone-to-direct renin concentration ratio (ADRR), which is calculated by direct renin concentration (DRC) measured by chemiluminescent immunoassay (CLIA), is proposed to replace ARR as the screening test method for PA. The purpose of the present study was to estimate the diagnostic accuracy and cutoff value of ADRR as screening test for PA.</AbstractText><AbstractText>450 hypertensive patients with suspected PA referred to hypertension center of our department were enrolled and underwent screening and confirmatory tests of PA. Plasma renin activity (PRA), DRC, and plasma aldosterone concentration (PAC) were measured by both RIA and CLIA simultaneously during screening and confirmatory test.</AbstractText><AbstractText>386 patients were diagnosed as primary hypertension (PH) and 64 patients as PA.
Within-patient correlation between PRA and DRC (r=0.88, P<0.001) and correlation between PAC measured by RIA and CLIA were high (r=0.80, P<0.001). The optimal cutoff value of ADRR was 2.93 (ng/dL)/(mU/L), sensitivity 80.33%, and specificity 92.11%. The optimal cutoff value of ARR was 25.28 (ng/dL)/(ng/mL/h), sensitivity 76.92%, and specificity 93.38%.</AbstractText><AbstractText>The optimal cutoff values of ADRR and ARR for screening PA are defined in this patient cohort with high sensitivity and specificity. Our results are of clinical importance for accelerating the extensive use of ADRR as a screening test for PA in daily practice.

Aldosterone Chemiluminescent ELISA Kit (1 Plate)
K052-C1 Arbor Assays 1x96 well plate 444 EUR

Aldosterone Chemiluminescent ELISA Kit (5 Plate)
K052-C5 Arbor Assays 5x96 well plate 1775 EUR

FTO Chemiluminescent Assay Kit
79344 BPS Bioscience 96 rxns. 765 EUR

G9a Chemiluminescent Assay Kit
52001L BPS Bioscience 96 rxns. 750 EUR

NSD3 Chemiluminescent Assay Kit
79358 BPS Bioscience 384 rxns. 1950 EUR

NSD2 Chemiluminescent Assay Kit
79359 BPS Bioscience 384 rxns. 1100 EUR

P300 Chemiluminescent Assay Kit
79705 BPS Bioscience 96 rxns. 465 EUR

GCN5 Chemiluminescent Assay Kit
50079L BPS Bioscience 96 rxns. 465 EUR

TET1 Chemiluminescent Assay Kit
50651 BPS Bioscience 96 rxns. 725 EUR

TET2 Chemiluminescent Assay Kit
50652 BPS Bioscience 96 rxns. 760 EUR

EZH2 Chemiluminescent Assay Kit
52009L BPS Bioscience 96 rxns. 1550 EUR

EZH1 Chemiluminescent Assay Kit
52079 BPS Bioscience 96 rxns. 1550 EUR

EZH2 Chemiluminescent Assay Kit
52085 BPS Bioscience 384 rxns. 2750 EUR

EZH1 Chemiluminescent Assay Kit
52990 BPS Bioscience 384 rxns. 4120 EUR

NSD2 Chemiluminescent Assay Kit
53009 BPS Bioscience 96 rxns. 750 EUR

NSD3 Chemiluminescent Assay Kit
53012 BPS Bioscience 96 rxns. 750 EUR

LSD1 Chemiluminescent Assay Kit
GWB-PS5F05 GenWay Biotech 96reactions Ask for price

cAMP ELISA Kit (Chemiluminescent)
MBS169108-5x96Assays MyBiosource 5x96Assays 2490 EUR

cAMP ELISA Kit (Chemiluminescent)
MBS169108-96Assays MyBiosource 96Assays 710 EUR

cAMP ELISA Kit (Chemiluminescent)
STA-501 Cell Biolabs 96 assays 428 EUR

cAMP ELISA Kit (Chemiluminescent)
STA-501-5 Cell Biolabs 5 x 96 assays 1740 EUR

cGMP ELISA Kit (Chemiluminescent)
STA-506 Cell Biolabs 96 assays 706.8 EUR

cGMP ELISA Kit (Chemiluminescent)
STA-506-5 Cell Biolabs 5 x 96 assays 2558.4 EUR

PRDM9 Chemiluminescent Assay Kit
79625 BPS Bioscience 96 rxns. 765 EUR

PARP7 Chemiluminescent Assay Kit
79729-1 BPS Bioscience 96 rxns. 1495 EUR

PARP7 Chemiluminescent Assay Kit
79729-2 BPS Bioscience 384 rxns. 2305 EUR

PRMT5 Chemiluminescent Assay Kit
52002L BPS Bioscience 96 rxns. 865 EUR

PRMT1 Chemiluminescent Assay Kit
52004L BPS Bioscience 96 rxns. 790 EUR

Diagnostic accuracy of aldosterone and renin measurement by chemiluminescent immunoassay and radioimmunoassay in primary aldosteronism.

Up to 50% of hypertensive patients should be screened for primary aldosteronism, using the aldosterone to renin (or plasma renin activity) ratio [aldosterone to active renin ratio (AARR) and aldosterone to plasma renin activity ratio (ARR), respectively]. Aim of the study was to prospectively compare the diagnostic accuracy of AARR (measured by chemiluminescent immunoassay) and ARR (measured by radioimmunoassay) as screening tests for primary aldosteronism and aldosterone assays (measured by chemiluminescence and radioimmunoassay) during confirmatory testing.
METHODS
One hundred patients were screened for primary aldosteronism and 34 underwent confirmatory testing. The cut-offs for ARR and AARR were 30 ng/dl/ng/ml/h and 3.7 ng/dl/mU/l, respectively. Patients with positive confirmatory test underwent subtype diagnosis.
RESULTS
Seventy-five patients were essential hypertensive patients, 15 had idiopathic hyperaldosteronism, five aldosterone-producing adenoma (APA) and five with undefined diagnosis. The AARR displayed a sensitivity of 90% and a specificity of 99%, the ARR had a sensitivity of 100% and a specificity of 73%. Of the two of 20 primary aldosteronism patients missed by AARR, none resulted affected by APA. All primary aldosteronism patients were correctly diagnosed by chemiluminescence at confirmatory testing. In the total sample of 168 measurements both the correlation for plasma renin activity with renin and for aldosterone in chemiluminescence and radioimmunoassay were highly significant (ρ = 0.70, P < 0.001 and ρ = 0.78, P < 0.001, respectively). On receiver operator characteristics curves, the area under the curve for AARR was 0.989 [95% confidence interval (CI) 0.97-1] and 0.934 for ARR (95% CI 0.89-0.98), which were not significantly different.
CONCLUSIONS
The automated aldosterone and renin chemiluminescent assay is a reliable alternative to the radioimmunometric method, especially for APA detection.

Radium 223 combined with new hormone therapies for the treatment of castrate-resistant metastatic prostate cancer: scientific evidence and sharing of our experience.

by
Radium 223 combined with new hormone therapies for the treatment of castrate-resistant metastatic prostate cancer: scientific evidence and sharing of our experience.
Presentation of the attention-grabbing case of a affected person affected by castrate-resistant prostate most cancers (CRPC) with bone metastasis, who obtained concomitant treatment with abiraterone acetate (AA) and radium-223. The affected person skilled important scientific enchancment in his high quality of life and ache aid after starting the aforementioned treatment, with out being affected by opposed toxicities.
Currently, the appropriate choice of sufferers to obtain radium-223 treatment remains to be a scientific problem in the case of CRPC with metastasis. In this text, we talk about the future prospects of this treatment, reviewing present evidence about concomitant therapies with radium-223 and its current state, primarily based upon the current suggestions from the Pharmacovigilance Risk Assessment Committee (PRAC), and the knowledge offered in the ERA-223 examine.
Based on our scientific expertise, we offer sensible orientation for the integration of this radiopharmaceutical in the therapeutic plan for this group of sufferers. We conclude, regardless of some of the constructive outcomes and our wonderful expertise, that it will be clever to attend for the outcomes of the scientific trials which are finding out the security and advantages of the combined use of radium-223 with new hormone therapies.
Bearing in thoughts that to this point, the solely revealed large-scale randomised trial that investigated the mixture of AR-axis-targeted remedy with Ra-223 is unfavourable, the harms of the mixture outweighed any advantages in ERA-223. Nonetheless, with a purpose to advocate whether or not or not this treatment must be used, it’s important to outline the affected person profile that would profit from this therapeutic possibility.
Radium 223 combined with new hormone therapies for the treatment of castrate-resistant metastatic prostate cancer: scientific evidence and sharing of our experience.
Radium 223 combined with new hormone therapies for the treatment of castrate-resistant metastatic prostate most cancers: scientific evidence and sharing of our expertise.