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multiple myeloma/prolina
Il collegamento viene salvato negli appunti
15 risultati
GSTM1 and codon 72 P53 polymorphism in multiple myeloma.
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The GSTM1 and GSTT1 genes reduce the effects of exposure to cytotoxic agents. Both genes have a null variant allele in which the entire gene is absent. On the other hand, a common polymorphism of the tumour suppressor P53 gene results in either arginine (A) or proline (P) at amino-acid position 72.
cis-4-[(18)F]-Fluoro-l-proline fails to detect peripheral tumors in humans.
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System A amino acid transport is increased in transformed and malignant cells. The amino acid 4-cis[(18)F]fluoro-l-proline (cis-[(18)F]FPro) has been shown to be a substrate of the System A amino acid carrier. In this pilot study, we investigated the diagnostic potential of cis-[(18)F]FPro in
Positive regulatory domain I binding factor 1 silences class II transactivator expression in multiple myeloma cells.
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The major histocompatibility complex (MHC) class II transactivator (CIITA) acts as a master switch to activate expression of the genes required for MHC-II antigen presentation. During B-cell to plasma cell differentiation, MHC-II expression is actively silenced, but the mechanism has been unknown.
Analysis of the Metabolic Characteristics of Serum Samples in Patients With Multiple Myeloma.
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Aims: This study aimed to identify potential, non-invasive biomarkers for diagnosis and monitoring of the progress in multiple myeloma (MM) patients. Methods: MM patients and age-matched healthy controls (HC) were recruited in Discovery phase and Validation phase, respectively. MM patients were
TP53 polymorphism in plasma cell myeloma.
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BACKGROUND
Significant and accessible predictive factors for bortezomib treatment in plasma cell myeloma (PCM) are still lacking. TP53 codon 72 polymorphism (P72R) results in proline (P) or arginine (R) at 72 amino acid position, which causes synthesis of proteins with distinct functions. The aims
Molecular features and expression of DAZAP2 in human multiple myeloma.
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BACKGROUND
In our previous study, we found that DAZAP2 was the most significantly down regulated gene when differential screening of complementary DNA (cDNA) chips were used to analyze mRNA isolated from bone marrow mononuclear cells from newly diagnosed multiple myeloma (MM) patients without
Pyk2 promotes tumor progression in multiple myeloma.
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Proline-rich tyrosine kinase 2 (Pyk2) is a member of the focal adhesion kinase family that has been recently linked to tumor development. However, its role in modulating multiple myeloma (MM) biology and disease progression remains unexplored. We first demonstrated that patients with MM present with
Targeting PYK2 mediates microenvironment-specific cell death in multiple myeloma.
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Multiple myeloma (MM) remains an incurable malignancy due, in part, to the influence of the bone marrow microenvironment on survival and drug response. Identification of microenvironment-specific survival signaling determinants is critical for the rational design of therapy and elimination of MM.
The iron chelator deferasirox induces apoptosis by targeting oncogenic Pyk2/β-catenin signaling in human multiple myeloma.
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Deregulated iron metabolism underlies the pathogenesis of many human cancers. Recently, low expression of ferroportin, which is the only identified non-heme iron exporter, has been associated with significantly reduced overall survival in multiple myeloma (MM); however, the altered iron metabolism
Mcl-1 regulation and its role in multiple myeloma.
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Among the Bcl-2 family, myeloid cell leukemia-1 (Mcl-1) distinguishes itself from the other pro-survival proteins by its ability to oppose to a wide variety of pro-apoptotic stimuli, short half-life, and presence of polypeptide sequences enriched in proline (P), glutamic acid (E), serine (S) and
Characterization of noncompetitive regulators of proteasome activity.
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The success of bortezomib, a competitive proteasome inhibitor and a drug approved to treat multiple myeloma, spurred interest in compounds targeting catalytic sites of the enzyme. The aim of this chapter, however, is to focus attention on the small molecule, natural or synthetic compounds binding
Liquid Chromatography Mass Spectrometry-Based Metabolite Pathway Analyses of Myeloma and Non-Hodgkin's Lymphoma Patients.
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OBJECTIVE
This study attempted to identify altered metabolism and pathways related to non-Hodgkin's lymphoma (NHL) and myeloma patients.
METHODS
In this retrospective study, we collected plasma samples from 11 patients-6 healthy controls with no evidence of any blood cancers and 5 patients with
Visualizing collagen proteolysis by peptide hybridization: From 3D cell culture to in vivo imaging.
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Degradation of the extracellular matrix (ECM) is one of the fundamental factors contributing to a variety of life-threatening or disabling pathological conditions. However, a thorough understanding of the degradation mechanism and development of new ECM-targeting diagnostics are severely hindered by
Allosteric effects of a monoclonal antibody against thrombin exosite II.
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We previously isolated a monoclonal antithrombin IgG from a patient with multiple myeloma [Colwell et al. (1997) Br. J. Haematol. 97, 219-226]. Using a panel of 55 surface mutants of recombinant thrombin, we now show that the epitope for the IgG most likely includes Arg-101, Arg-233, and Lys-236 in
The cytoplasmic tyrosine kinase Pyk2 as a novel effector of fibroblast growth factor receptor 3 activation.
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Activating mutations within fibroblast growth factor receptor 3 (FGFR3), a receptor tyrosine kinase, are responsible for human skeletal dysplasias including achondroplasia and the neonatal lethal syndromes thanatophoric dysplasia types I and II. Several of these same FGFR3 mutations have also been
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