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Circulating Biomarker (circulating + biomarker)
Selected AbstractsCirculating biomarkers for vascular endothelial growth factor inhibitors in renal cell carcinoma,CANCER, Issue S10 2009Amado J. Zurita MD Abstract In recent years, there has been significant progress in the clinical development and application of antiangiogenic therapies in renal cell carcinomas, particularly inhibitors of the vascular endothelial growth factor (VEGF) pathway. Despite this progress, no validated methods are currently available for identifying which patients are most likely to respond to treatment or experience toxic effects, selecting the optimal dose, or determining whether the intended molecular target has been effectively inhibited. However, recent studies have suggested that some of the biomarkers currently under investigation in clear cell renal cell carcinoma for VEGF pathway inhibitors are promising. These biomarkers include circulating proangiogenic factors and receptors; markers of hypoxia and endothelial damage; and cellular populations in peripheral blood, such as circulating endothelial cells. Further preclinical and translational validation studies are still needed to determine their practical utility in the clinical setting. Cancer 2009;115(10 suppl):2346-54. © 2009 American Cancer Society. [source] Serum Cardiac Troponin I Concentration in Dogs with Precapillary and Postcapillary Pulmonary HypertensionJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2010C. Guglielmini Background: Pulmonary hypertension (PH) is a disease condition leading to right-sided cardiac hypertrophy and, eventually, right-sided heart failure. Cardiac troponin I (cTnI) is a circulating biomarker of cardiac damage. Hypothesis: Myocardial damage can occur in dogs with precapillary and postcapillary PH. Animals: One hundred and thirty-three dogs were examined: 26 healthy controls, 42 dogs with mitral valve disease (MVD) without PH, 48 dogs with pulmonary hypertension associated with mitral valve disease (PH-MVD), and 17 dogs with precapillary PH. Methods: Prospective, observational study. Serum cTnI concentration was measured with a commercially available immunoassay and results were compared between groups. Results: Median cTnI was 0.10 ng/mL (range 0.10,0.17 ng/mL) in healthy dogs. Compared with the healthy population, median serum cTnI concentration was increased in dogs with precapillary PH (0.25 ng/mL; range 0.10,1.9 ng/mL; P < .001) and in dogs with PH-MVD (0.21 ng/mL; range 0.10,2.10 ng/mL; P < .001). Median serum cTnI concentration of dogs with MVD (0.12 ng/mL; range 0.10,1.00 ng/mL) was not significantly different compared with control group and dogs with PH-MVD. In dogs with MVD and PH-MVD, only the subgroup with decompensated PH-MVD had significantly higher cTnI concentration compared with dogs with compensated MVD and PH-MVD. Serum cTnI concentration showed significant modest positive correlations with the calculated pulmonary artery systolic pressure in dogs with PH and some echocardiographic indices in dogs with MVD and PH-MVD. Conclusions and Clinical Importance: Serum cTnI is high in dogs with either precapillary and postcapillary PH. Myocardial damage in dogs with postcapillary PH is likely the consequence of increased severity of MVD. [source] Expansion of circulating T cells resembling follicular helper T cells is a fixed phenotype that identifies a subset of severe systemic lupus erythematosusARTHRITIS & RHEUMATISM, Issue 1 2010Nicholas Simpson Objective In the sanroque mouse model of lupus, pathologic germinal centers (GCs) arise due to increased numbers of follicular helper T (Tfh) cells, resulting in high-affinity anti,double-stranded DNA antibodies that cause end-organ inflammation, such as glomerulonephritis. The purpose of this study was to examine the hypothesis that this pathway could account for a subset of patients with systemic lupus erythematosus (SLE). Methods An expansion of Tfh cells is a causal, and therefore consistent, component of the sanroque mouse phenotype. We validated the enumeration of circulating T cells resembling Tfh cells as a biomarker of this expansion in sanroque mice, and we performed a comprehensive comparison of the surface phenotype of circulating and tonsillar Tfh cells in humans. This circulating biomarker was enumerated in SLE patients (n = 46), Sjögren's syndrome patients (n = 17), and healthy controls (n = 48) and was correlated with disease activity and end-organ involvement. Results In sanroque mice, circulating Tfh cells increased in proportion to their GC counterparts, making circulating Tfh cells a feasible human biomarker of this novel mechanism of breakdown in GC tolerance. In a subset of SLE patients (14 of 46), but in none of the controls, the levels of circulating Tfh cells (defined as circulating CXCR5+CD4+ cells with high expression of Tfh-associated molecules, such as inducible T cell costimulator or programmed death 1) were increased. This cellular phenotype did not vary with time, disease activity, or treatment, but it did correlate with the diversity and titers of autoantibodies and with the severity of end-organ involvement. Conclusion These findings in SLE patients are consistent with the autoimmune mechanism in sanroque mice and identify Tfh effector molecules as possible therapeutic targets in a recognizable subset of patients with SLE. [source] Inflammatory Biomarkers are not Predictive of Intermediate-term Risk of Ventricular Tachyarrhythmias in Stable CHF PatientsCLINICAL CARDIOLOGY, Issue 8 2007Yuval Konstantino M.D. Abstract Background: Elevated levels of inflammatory biomarkers and brain natriuretic peptide (BNP) are associated with increased mortality in patients with heart failure (HF). Hypothesis: The aim of the current study was to assess the correlation between circulating biomarkers and ventricular tachyarrhythmias among patients with HF. Methods: Blood samples from 50 stable ambulatory HF patients with moderate to severe systolic left ventricular (LV) dysfunction and an implantable cardioverter defibrillator (ICD) were analyzed for interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-,), high-sensitivity C-reactive protein (hsCRP) and BNP. Thereafter, the patients were followed for a mean period of 152 ± 44 days, during which ventricular tachyarrhythmias were recorded by the ICDs. Results: Follow-up data were obtained from 47 patients. Of them, 45 (96%) had ischemic cardiomyopathy, 38 (81%) had New York Heart Association class I,II, 43 (91%) were males, and the mean age was 68.6 ± 11.1 years. During follow-up, 5 patients (11%) had nonsustained ventricular tachycardia (NSVT), 6 patients (13%) had sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) and 36 patients (76%) had no events. The circulating biomarkers' levels upon enrollment were not significantly different between patients who subsequently had NSVT or VT/VF and patients who were free of events. Conclusions: No correlation was found between plasma levels of IL-6, TNF-,, hsCRP and BNP and ventricular arrhythmic events among stable HF patients during an intermediate term follow-up of 5.1 months. Further studies are still required to assess the association between these biomarkers and long-term risk of ventricular tachyarrhythmia. Copyright © 2007 Wiley Periodicals, Inc. [source] | ||||||||||