Pharmacogenomics of bortezomib test-dosing identifies hyperexpression of proteasome genes, especially PSMD4, as novel high-risk feature in myeloma treated with Total Therapy 3
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Trial Watch: Proteasomal inhibitors for anticancer therapyBortezomib resistance can be reversed by induced expression of plasma cell maturation markers in a mouse in vitro model of multiple myelomaProof of the concept to use a malignant B cell line drug screen strategy for identification and weight of melphalan resistance genes in multiple myelomaUtilization of translational bioinformatics to identify novel biomarkers of bortezomib resistance in multiple myelomaAdvances in understanding prognosis in myeloma.Metronomic therapy is an effective salvage treatment for heavily pre-treated relapsed/refractory multiple myelomaAnalysis of CD34+ cell collection using two mobilization regimens for newly diagnosed multiple myeloma patients reveals the separate impact of mobilization and collection variablesStandard and novel imaging methods for multiple myeloma: correlates with prognostic laboratory variables including gene expression profiling data.Leveraging the new with the old: providing a framework for the integration of historic microarray studies with next generation sequencing.Towards the integration, annotation and association of historical microarray experiments with RNA-seqEx vivo-expanded natural killer cells demonstrate robust proliferation in vivo in high-risk relapsed multiple myeloma patientsRemoving batch effects from purified plasma cell gene expression microarrays with modified ComBat.The flow cytometry-defined light chain cytoplasmic immunoglobulin index and an associated 12-gene expression signature are independent prognostic factors in multiple myeloma.Primary plasma cell leukemia: clinical and laboratory presentation, gene-expression profiling and clinical outcome with Total Therapy protocols.Prediction of high- and low-risk multiple myeloma based on gene expression and the International Staging System.Mitochondrial-Targeted Decyl-Triphenylphosphonium Enhances 2-Deoxy-D-Glucose Mediated Oxidative Stress and Clonogenic Killing of Multiple Myeloma CellsThe amplification of 1q21 is an adverse prognostic factor in patients with multiple myeloma in a Chinese populationMTDH is an oncogene in multiple myeloma, which is suppressed by Bortezomib treatment.Treatment of multiple myeloma with high-risk cytogenetics: a consensus of the International Myeloma Working Group.Improvement in long-term outcomes with successive Total Therapy trials for multiple myeloma: are patients now being cured?Why proteasome inhibitors cannot ERADicate multiple myeloma.Chromosome 1q21 gains confer inferior outcomes in multiple myeloma treated with bortezomib but copy number variation and percentage of plasma cells involved have no additional prognostic value.Gambogenic acid synergistically potentiates bortezomib-induced apoptosis in multiple myeloma.The use of molecular-based risk stratification and pharmacogenomics for outcome prediction and personalized therapeutic management of multiple myeloma.Latest advances and current challenges in the treatment of multiple myeloma.Emerging biological insights and novel treatment strategies in multiple myeloma.Molecular profiling of multiple myeloma: from gene expression analysis to next-generation sequencing.Perspectives in the treatment of multiple myeloma.Biologic frontiers in multiple myeloma: from biomarker identification to clinical practice.The impact of intra-clonal heterogeneity on the treatment of multiple myeloma.Proteasome inhibitors - molecular basis and current perspectives in multiple myeloma.Metronomic chemotherapy.Recent advances and future directions in targeting the secretory apparatus in multiple myeloma.Proteasome ubiquitin receptor PSMD4 is an amplification target in breast cancer and may predict sensitivity to PARPi.Expression Profiles of the Individual Genes Corresponding to the Genes Generated by Cytotoxicity Experiments with Bortezomib in Multiple Myeloma.Profiling bortezomib resistance identifies secondary therapies in a mouse myeloma model.Molecular mechanisms of acquired proteasome inhibitor resistance.Gene signature combinations improve prognostic stratification of multiple myeloma patients.Gain of chromosome 1q portends worse prognosis in multiple myeloma despite novel agent-based induction regimens and autologous transplantation.The degradation of p53 and its major E3 ligase Mdm2 is differentially dependent on the proteasomal ubiquitin receptor S5a.
P2860
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P2860
Pharmacogenomics of bortezomib test-dosing identifies hyperexpression of proteasome genes, especially PSMD4, as novel high-risk feature in myeloma treated with Total Therapy 3
description
2011 nî lūn-bûn
@nan
2011 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Pharmacogenomics of bortezomib ...... a treated with Total Therapy 3
@ast
Pharmacogenomics of bortezomib ...... a treated with Total Therapy 3
@en
type
label
Pharmacogenomics of bortezomib ...... a treated with Total Therapy 3
@ast
Pharmacogenomics of bortezomib ...... a treated with Total Therapy 3
@en
prefLabel
Pharmacogenomics of bortezomib ...... a treated with Total Therapy 3
@ast
Pharmacogenomics of bortezomib ...... a treated with Total Therapy 3
@en
P2093
P2860
P50
P1433
P1476
Pharmacogenomics of bortezomib ...... a treated with Total Therapy 3
@en
P2093
Bijay Nair
Christoph J Heuck
Erming Tian
Ichiro Hanamura
John Crowley
John D Shaughnessy
Joshua Epstein
Owen Stephens
Pingping Qu
Qing Zhang
P2860
P304
P356
10.1182/BLOOD-2010-12-328252
P407
P577
2011-05-31T00:00:00Z