Research Topics
Genomes and Genes | Thomas O'HareSummaryAffiliation: Oregon Health and Science University Country: USA Publications
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Publications
In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutantsThomas O'Hare
Howard Hughes Medical Institute, Oregon Health and Science University Cancer Institute, Portland 97239, USA
Cancer Res 65:4500-5. 2005..Thus, both inhibitors hold promise for treating imatinib-refractory CML...- Inhibition of wild-type and mutant Bcr-Abl by AP23464, a potent ATP-based oncogenic protein kinase inhibitor: implications for CMLThomas O'Hare
Howard Hughes Medical Institute, Oregon Health and Science University, L592, 3181 SW Sam Jackson Park Rd, Portland, OR 97239, USA
Blood 104:2532-9. 2004..The potency of AP23464 against imatinib mesylate-refractory Bcr-Abl and its distinct binding mode relative to imatinib mesylate warrant further investigation of AP23464 for the treatment of CML... 
Targeting the BCR-ABL signaling pathway in therapy-resistant Philadelphia chromosome-positive leukemiaThomas O'Hare
Division of Hematology and Medical Oncology, Oregon Health and Science University Knight Cancer Institute, Portland, Oregon, USA
Clin Cancer Res 17:212-21. 2011....- A simple method for determining K(A)s of both low and high affinity IgG antibodiesT O'Hare
Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland 97201, USA
J Immunol Methods 218:161-7. 1998..The K(A) is obtained by Scatchard analysis... - Combined Abl inhibitor therapy for minimizing drug resistance in chronic myeloid leukemia: Src/Abl inhibitors are compatible with imatinibThomas O'Hare
Howard Hughes Medical Institute, Oregon Health and Science University, Portland 97239, USA
Clin Cancer Res 11:6987-93. 2005..As combination therapy is frequently used to prevent emergence of resistance, the combination of imatinib with an inhibitor of imatinib-resistant Bcr-Abl mutants (e.g., Src/Abl inhibitors AP23848 and BMS-354825) was investigated... - New Bcr-Abl inhibitors in chronic myeloid leukemia: keeping resistance in checkThomas O'Hare
Oregon Health and Science University Cancer Institute, Howard Hughes Medical Institute, Portland, Oregon 97239, USA
Expert Opin Investig Drugs 17:865-78. 2008..Improved Abl inhibitor therapies will be useful in achieving maximum disease control but a clinical T315I inhibitor remains a high priority... 
A BCR-ABL mutant lacking direct binding sites for the GRB2, CBL and CRKL adapter proteins fails to induce leukemia in miceKara J Johnson
Division of Hematology and Medical Oncology, Oregon Health and Science University Knight Cancer Institute, Portland, Oregon, United States of America
PLoS ONE 4:e7439. 2009..Our data suggest that inhibition of BCR-ABL-induced leukemia by disrupting protein interactions could be possible, but would require blocking of multiple sites...- AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistanceThomas O'Hare
Division of Hematology and Medical Oncology, Oregon Health and Science University Knight Cancer Institute, Portland, OR 97239, USA
Cancer Cell 16:401-12. 2009..Our work supports clinical evaluation of AP24534 as a pan-BCR-ABL inhibitor for treatment of CML... - The ABL switch control inhibitor DCC-2036 is active against the chronic myeloid leukemia mutant BCR-ABLT315I and exhibits a narrow resistance profileChristopher A Eide
Oregon Health and Science University, Knight Cancer Institute, Portland, OR, USA
Cancer Res 71:3189-95. 2011..Taken together, these findings support continued evaluation of DCC-2036 as an important new agent for treatment-refractory CML... - Activating alleles of JAK3 in acute megakaryoblastic leukemiaDenise K Walters
Howard Hughes Medical Institute, Portland, Oregon 97239, USA
Cancer Cell 10:65-75. 2006..These findings illustrate the biological importance of gain-of-function JAK3 mutations in leukemogenesis and demonstrate the utility of proteomic approaches to identifying clinically relevant mutations... - RNAi screening of the tyrosine kinome identifies therapeutic targets in acute myeloid leukemiaJeffrey W Tyner
Division of Hematology and Medical Oncology, Oregon Health and Science University Cancer Institute, Portland, USA
Blood 111:2238-45. 2008..This technique, with additional development, might eventually offer the potential to match specific therapies with individual patients based on a functional assay... - Absence of SKP2 expression attenuates BCR-ABL-induced myeloproliferative diseaseAnupriya Agarwal
Division of Hematology and Oncology, Oregon Health and Science University Cancer Institute, Portland, OR 97239, USA
Blood 112:1960-70. 2008..Hence, stabilization of p27 by inhibiting its recognition by SCF(SKP2) may be therapeutically useful... - RNAi screen for rapid therapeutic target identification in leukemia patientsJeffrey W Tyner
Division of Hematology and Medical Oncology, Oregon Health and Science University Knight Cancer Institute, Portland, OR 97239, USA
Proc Natl Acad Sci U S A 106:8695-700. 2009..Combination of this technique with whole-genome sequencing will represent an ideal tool for oncogenic target identification such that specific therapies can be matched with individual patients... - Acute dasatinib exposure commits Bcr-Abl-dependent cells to apoptosisJennifer L Snead
Division of Hematology and Medical Oncology, Oregon Health and Science University Knight Cancer Institute, Portland, OR 97239, USA
Blood 114:3459-63. 2009..Furthermore, they challenge the widely held notion that continuous target inhibition is required for optimal efficacy of kinase inhibitors... - SGX393 inhibits the CML mutant Bcr-AblT315I and preempts in vitro resistance when combined with nilotinib or dasatinibThomas O'Hare
Division of Hematology and Medical Oncology, Oregon Health and Science University Cancer Institute, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA
Proc Natl Acad Sci U S A 105:5507-12. 2008..These findings suggest that combination of a T315I inhibitor with the current clinically used inhibitors may be useful for reduction of Bcr-Abl mutants in Philadelphia chromosome-positive leukemia... - The BCR-ABL35INS insertion/truncation mutant is kinase-inactive and does not contribute to tyrosine kinase inhibitor resistance in chronic myeloid leukemiaThomas O'Hare
Division of Hematology and Medical Oncology, Oregon Health and Science University Knight Cancer Institute, Portland, USA
Blood 118:5250-4. 2011.... - TNFα facilitates clonal expansion of JAK2V617F positive cells in myeloproliferative neoplasmsAngela G Fleischman
Division of Hematology and Medical Oncology, Oregon Health and Science University Knight Cancer Institute, Portland, OR, USA
Blood 118:6392-8. 2011.... - New strategies for the first-line treatment of chronic myeloid leukemia: can resistance be avoided?Jennifer L Snead
Oregon Health and Science University Cancer Institute, Portland, OR, USA
Clin Lymphoma Myeloma 8:S107-17. 2008..Herein, we review current and emerging paradigms for using Abl kinase inhibitors to achieve maximal disease control and strategies to eradicate disease by targeting leukemic stem cells... - Recovering antibody secretion using a hapten ligand as a chemical chaperoneG D Wiens
Department of Molecular Microbiology and Immunology, Oregon Health and Science University, Portland, Oregon 97201 3098, USA
J Biol Chem 276:40933-9. 2001.... - Mutation of a single conserved residue in VH complementarity-determining region 2 results in a severe Ig secretion defectG D Wiens
Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland, OR 97201, USA
J Immunol 167:2179-86. 2001..These results represent the first demonstration that single somatic mutations in V(H) residues can impair Ig secretion and suggest one reason for the conservation of Ile51 in so many Ig VH... - Harmful somatic mutations: lessons from the dark sideG D Wiens
Department of Molecular Microbiology, Oregon Health Sciences University, Portland 97201, USA
Immunol Rev 162:197-209. 1998..Here we review our recent findings in understanding the structural and functional consequences of V-region mutation... - Clonal diversity, somatic mutation, and immune memory to phosphocholine-keyhole limpet hemocyaninM P Stenzel-Poore
Department of Microbiology and Immunology, Oregon Health Sciences University, Portland 97201
J Immunol 143:4123-33. 1989..From these findings it appears that somatic mutation plays a major role in anti-PC-keyhole limpet hemocyanin memory development because all 14 antibodies displayed changes from germ-line sequences... - Association of human transferrin receptor with GABARAPFrank Green
Department of Cell and Developmental Biology, L215, Oregon Health and Science University, 3181 SW Sam Jackson Park Rd, Portland, OR 97201 3098, USA
FEBS Lett 518:101-6. 2002..Our results show that GABARAP plays a more general role outside the confines of neuronal cells and GABA(A) receptors... - Single particle quantum dot imaging achieves ultrasensitive detection capabilities for Western immunoblot analysisBenjamin Scholl
Department of Biomedical Engineering, Oregon Health and Science University, Portland, OR 97239, USA
ACS Nano 3:1318-28. 2009.... - A genetic model of stress displays decreased lymphocytes and impaired antibody responses without altered susceptibility to Streptococcus pneumoniaeS E Murray
Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland, OR 97201, USA
J Immunol 167:691-8. 2001..This increase in number of neutrophils may compensate for the depressed IgG response, allowing adequate host defense during chronic stress... - Natural auto- and polyreactive antibodies differing from antigen-induced antibodies in the H chain CDR3C Chen
Department of Microbiology and Immunology, Oregon Health Sciences University, Portland 97201
J Immunol 147:2359-67. 1991..The results suggest that CDR3 of the H chain may play a critical role in distinguishing poly- from monospecific combining sites in natural and Ag-induced antibodies... - Cutting edge: proteasome involvement in the degradation of unassembled Ig light chainsT O'Hare
Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland 97201, USA
J Immunol 163:11-4. 1999..To our knowledge, we provide the first direct evidence supporting a new paradigm for removal of nonsecreted Ig L chains via dislocation to cytosolic proteasomes...