WorldCat Identities

Druker, Brian J.

Overview
Works: 15 works in 24 publications in 1 language and 385 library holdings
Roles: Speaker
Publication Timeline
.
Most widely held works about Brian J Druker
  • DNA( Visual )
 
moreShow More Titles
fewerShow Fewer Titles
Most widely held works by Brian J Druker
Imatinib as a paradigm of targeted cancer therapies by Brian J Druker( Visual )

2 editions published in 2007 in English and held by 51 WorldCat member libraries worldwide

Audio-visual presentation : Clinical description of chronic myeloid leukemia (CML) ; Molecular pathogenesis of CML ; The BCR-ABL tyrosine kinase as a therapeutic target ; Preclinical and clinical development of the ABL tyrosine kinase inhibitor, imatinib ; Mechanisms of resistance to imatinib ; Development of novel ABL tyrosine kinase inhibitors for imatinib-resistant CML ; Imatinib and gastrointestinal stromal tumor ; Extending the imatinib paradigm ; Lessons learned from the clinical trials of imatinib
Mechanisms of Disease Persistence in Chronic Myelogenous Leukemia( Book )

2 editions published in 2007 in English and held by 2 WorldCat member libraries worldwide

Disease persistence is the main issue faced by CML patients on therapy with imatinib and eradication of persistent malignant cells will be critical for the long-term success of kinase inhibitor therapy. Mechanisms underlying acquired resistance to imatinib have been extensively studied and the manner by which mutations of the Bcr-Abl kinase domain can reduce or eliminate sensitivity of CML cells to imatinib has been well characterized. Disease persistence in responding patients, in contrast,is still poorly understood. We sought to identify and extensively characterize hematopoietic stem cells responsible for disease persistence and explore their mechanisms of imatinib resistance. Using in vitro culture of primary CML progenitor cells, we identified both quiescent and cycling cells capable of surviving in the presence of imatinib. We observed inhibition of tyrosine phosphorylation by imatinib in phenotypically-defined CML stem cells and quiescent stem cells, and cells surviving in vitro culture, suggesting a Bcr-Abl independent mechanism of survival. To apply information gained from in vitro culture to persistent cell populations in treated CML patients, we attempted to isolate Bcr-Abl positive cells from patients in cytogenetic remission. Although persistent CML cells may reside within the stem cell compartment, techniques of stem cell enrichment did not lead to enrichment of CML cells. We therefore explored techniques for Bcr-Abl-specific detection to facilitate these studies, including creation of a Bcr-Abl junction-specific antibody, development of a Bcr-Abl mRNA junction-specific molecular beacon and analysis of potential markers of CML cells. The detailed analysis of primary samples is technically challenging, but is essential for an understanding of disease persistence and may allow identification of novel drug targets or methods to sensitize resistant cells to imatinib or alternative Bcr-Abl kinase inhibitors
Mechanisms of Disease Persistence in Chronic Myelogenous Leukemia (CML)( Book )

2 editions published in 2006 in English and held by 2 WorldCat member libraries worldwide

Disease persistence is the main issue faced by CML patients on therapy with imatinib and eradication of persistent malignant cells will be critical for the longterm success of kinase inhibitor therapy. Mechanisms underlying acquired resistance to imatinib have been extensively studied and the manner by which mutations of the Bcr-Abl kinase domain can reduce or eliminate sensitivity of CML cells to imatinib has been well characterized. Disease persistence in responding patients, in contrast, is still poorly understood. We sought to identify and extensively characterize hematopoietic stem cells responsible for disease persistence and explore their mechanisms of imatinib resistance. Using in vitro culture of primary CML progenitor cells, we identified both quiescent and cycling cells capable of surviving in the presence of imatinib. We observed inhibition of tyrosine phosphorylation by imatinib in surviving cells, suggesting a Bcr-Abl independent mechanism of survival. To apply information gained from in vitro culture to persistent cell populations in treated CML patients, we attempted to isolate Bcr-Abl positive cells from patients in cytogenetic remission. Although persistent CML cells may reside within the stem cell compartment, techniques of stem cell enrichment did not lead to enrichment of CML cells. We are therefore developing techniques for Bcr-Abl-specific detection to facilitate these studies, including creation of a Bcr-Abl junction-specific antibody, development of a Bcr-Abl mRNA junction-specific molecular beacon and analysis of potential markers of CML cells. Evaluation of the utility of these techniques in primary cells is ongoing. The detailed analysis of primary samples is technically challenging, but is essential for an understanding of disease persistence and may allow identification of novel drug targets or methods to sensitize resistant cells to imatinib or alternative Bcr-Abl kinase inhibitors
STI571, a tyrosine kinase inhibitor for the treatment of CML : validating the promise of molecularly targeted therapy by Brian J Druker( Visual )

1 edition published in 2002 in English and held by 1 WorldCat member library worldwide

Using CML as an example, Dr. Druker discusses translational research, how it unfolds and where it leads: " ... we start by defining a clinical entity, we then understand its molecular pathogenesis, and ideally create a therapeutic agent based on that molecular pathogenic event."
Imatinib as a paradigm of targeted cancer therapies by Brian J Druker( Book )

1 edition published in 2007 in English and held by 1 WorldCat member library worldwide

Novel Method Enabling the Use of Cryopreserved Primary Acute Myeloid Leukemia Cells in Functional Drug Screens( )

1 edition published in 2017 in English and held by 1 WorldCat member library worldwide

Abstract : The ability to assess antileukemic drug activity on primary patient samples is a powerful tool in determining potential drug targets and selection of therapeutic agents with biological and functional rationale. We previously established small molecule inhibitor screens for use on freshly isolated leukemia cells for this purpose. Here we describe a method that produces functional small molecule inhibitor screening results using cryopreserved primary acute myeloid leukemia cells. This method was established to take advantage of biorepositories containing archival material, such as those established by the Children's Oncology Group, and to enable validation of potential pathway dependencies uncovered by genomic analysis. Various conditions used to thaw and culture cryopreserved specimens were assessed for effect on viability, differentiation, and the ability to recapitulate sensitivity results obtained on fresh samples. The most reproducible results were obtained by quick-thawing and culturing samples in cytokine rich media before performing drug screens. Our data suggest that cytokine-enriched media aids in maintaining the viability and numbers required to perform functional analysis on cryopreserved leukemia cells. This method can aid in producing informative data on therapeutic targeting and precision medicine efforts in leukemia by making use of biorepositories and bio banks. Abstract : Supplemental Digital Content is available in the text
Targeting cancer in the 21st century by Brian J Druker( Visual )

1 edition published in 2002 in English and held by 1 WorldCat member library worldwide

Using CML as an example, Dr. Druker discusses how, if one can understand what causes cancer, one can treat or even prevent it
Imatinib as a paradigm of targeted cancer therapies by Brian J Druker( )

1 edition published in 2007 in English and held by 0 WorldCat member libraries worldwide

Audio-visual presentation: Clinical description of chronic myeloid leukemia (CML) -- Molecular pathogenesis of CML -- The BCR-ABL tyrosine kinase as a therapeutic target -- Preclinical and clinical development of the ABL tyrosine kinase inhibitor, imatinib -- Mechanisms of resistance to imatinib -- Development of novel ABL tyrosine kinase inhibitors for imatinib-resistant CML -- Imatinib and gastrointestinal stromal tumor -- Extending the imatinib paradigm -- Lessons learned from the clinical trials of imatinib
 
Audience Level
0
Audience Level
1
  Kids General Special  
Audience level: 0.27 (from 0.17 for DNA / ... to 1.00 for Imatinib a ...)

Alternative Names
Brian Druker Amerikaans oncoloog

Brian Druker amerykański lekarz onkolog

Brian Druker médecin américain

Brian Druker médico estadounidense

Brian Druker US-amerikanischer Mediziner und Krebsforscher

Друкер, Брайан

ബ്രയാൻ ജെ. ഡ്രൂകർ

ブライアン・ドラッカー

布莱恩·德鲁克尔

Languages
English (24)