Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.1.1 (asparaginase)
 2,695 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The C-reactive protein is a generally recognized marker of inflammation and bacterial infection. However, issue of diagnostic effectiveness of this indicator is still open-ended in case of patients with oncologic hematological diseases. The level of C-reactive protein can increase under neoplastic processes. On the contrary, the inhibition of immune response observed under cytoplastic therapy can decrease synthesis of this protein. The study was organized to establish levels of C-reactive protein as markers of infection in adult patients with acute lymphoblastic leucosis under application of chemotherapy and to evaluate their diagnostic effectiveness. The sampling included 34 patients with acute lymphoblastic leucosis all patients had infectious complications at various stages of treatment. The levels of C-reactive protein in groups of patients with localized infections (mucositis, abscess, pneumonia, etc.) or fever of unknown genesis had no statistical differences but were reliably higher in patients without infectious complications. The concentrations of C-reactive protein in patients with syndrome of systemic inflammatory response and sepsis had no differences. At the same time, level of C-reactive protein under systemic infection (syndrome of systemic inflammatory response, sepsis) was reliably higher than in case of localized infection. The diagnostically reliable levels of C-reactive protein were established as follows: lower than 11 mg/l--infectious complications are lacking; higher than 11 mg/l--availability of infectious process; higher than 82 mg/l--generalization of infection. The given levels are characterized by high diagnostic sensitivity (92% and 97% correspondingly) and specificity (97% and 97%) when patients receive therapy without application of L-asparaginase. At the stages of introduction of this preparation effecting protein synthesizing function of liver sensitivity of proposed criteria are decreased (69% and 55% correspondingly). However; due to high specificity (100% and 96%) their diagnostic effectiveness remains high.
 ...
PMID:[The evaluation of sensitivity and specificity of technique of detection of C-reactive protein under diagnostic of infectious complications in patients with acute lymphoblastic leucosis receiving chemotherapy]. 2585 Feb 39

Natural-killer/T cell lymphoma (NKTCL) is the most common extranodal lymphoma with highly aggressive clinical outcome. System biology techniques provide novel insights into the pathogenesis, risk stratification, and clinical management in NKTCL. Comparative genomic hybridization analysis reveal most frequent deletion of chromosome 6q21. Whole-exome sequencing studies identify recurrent somatic gene mutations, involving RNA helicases, tumor suppressors, JAK-STAT pathway molecules, and epigenetic modifiers. Genome-wide association study reports strongest association of HLA-DPB1 rs9277378 with lymphomagenesis. Alterations of oncogenic signaling pathways as well as epigenetic dysregulation of microRNA and long non-coding RNAs are also observed in NKTCL. Epstein-Barr virus (EBV) is the major etiology of NKTCL and the pathogenic mechanism remains unclear. Different risk stratification models are proposed based on clinical parameters (IPI, PINK, and PINK-E, etc.) or biomarkers (Ki67, C-reactive protein level, and EBV DNA, etc.). Therapeutic strategies vary according to disease stage, including radiotherapy, asparaginase-based chemotherapy, hematopoietic stem-cell transplantation, targeted therapy (immune checkpoints inhibitors, and histone deacetylation inhibitors, etc.). Future investigations will be emphasized on EBV-related pathogenesis of NKTCL, prognostic and therapeutic biomarkers, as well as multi-center clinical trials, so as to optimize personalized treatment of NKTCL in the era of precision medicine.
 ...
PMID:What we should know about natural killer/T-cell lymphomas. 3118 36