Professor, Internal Medicine, University of Utah School of Medicine
Hematology
Dr. Michael W. Deininger, MD
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Michael Deininger practices Hematology. Dr. Michael W. Deininger is a published doctor as well. He has 69 publications published. The latest was: A phase II study of the efficacy, safety, and determinants of response to 5-azacitidine (Vidaza) in patients with chronic myelomonocytic leukemia. Doctor Michael W. Deininger, MD is registered with Medicare and accepts Medicare payments.
Publications
- A phase II study of the efficacy, safety, and determinants of response to 5-azacitidine (Vidaza®) in patients with chronic myelomonocytic Leukemia.
- Extreme mutational selectivity of axitinib limits its potential use as a targeted therapeutic for BCR-ABL1-positive Leukemia.
- The effect of long-term ruxolitinib treatment on JAK2p.V617F allele burden in patients with myelofibrosis.
- β-Catenin is required for intrinsic but not extrinsic BCR-ABL1 kinase-independent resistance to tyrosine kinase inhibitors in chronic myeloid Leukemia.
- Combined STAT3 and BCR-ABL1 inhibition induces synthetic lethality in therapy-resistant chronic myeloid Leukemia.
- shRNA library screening identifies nucleocytoplasmic transport as a mediator of BCR-ABL1 kinase-independent resistance.
- Radotinib is an effective inhibitor of native and kinase domain-mutant BCR-ABL1.
- A coiled-coil mimetic intercepts BCR-ABL1 dimerization in native and kinase-mutant chronic myeloid Leukemia.
- Mutations in G protein β subunits promote transformation and kinase inhibitor resistance.
- Novel insights into the biology and treatment of Chronic myeloproliferative neoplasms.
- BCR-ABL1 promotes Leukemia by converting p27 into a cytoplasmic oncoprotein.
- BCR-ABL1 Compound Mutations Combining Key Kinase Domain Positions Confer Clinical Resistance to Ponatinib in Ph Chromosome-Positive Leukemia.
- The current status of ponatinib in the treatment of chronic myeloid Leukemia.
- Imatinib 800Â mg daily induces Deeper molecular responses than imatinib 400Â mg daily: results of SWOG S0325, an intergroup randomized PHASE II trial in newly diagnosed ...
- Chronic myelogenous Leukemia, version 1.2014.
- A Phase 2 Trial of Ponatinib in Philadelphia Chromosome-Positive Leukemias.
- Comparison of placebo and best available therapy for the treatment of myelofibrosis in the phase 3 COMFORT studies.
- KIT signaling governs differential sensitivity of mature and primitive CML progenitors to tyrosine kinase inhibitors.
- Oncogenic CSF3R mutations in chronic neutrophilic Leukemia and atypical CML.
- Analysis of the potential effect of ponatinib on the QTc interval in patients with refractory hematological malignancies.
- Threshold levels of ABL tyrosine kinase inhibitors retained in chronic myeloid Leukemia cells define commitment to apoptosis.
- Effect of Ruxolitinib Therapy on Myelofibrosis-Related Symptoms and Other Patient-Reported Outcomes in COMFORT-I: A Randomized, Double-Blind, Placebo-Controlled Trial.
- The clinical benefit of ruxolitinib across patient subgroups: analysis of a placebo-controlled, Phase III study in patients with myelofibrosis.
- New concepts for CML clonality.
- Kinase Pathway Dependence in Primary Human Leukemias Determined by Rapid Inhibitor Screening.
- BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships.
- Effects of plerixafor in combination with BCR-ABL kinase inhibition in a murine model of CML.
- Development of an effective therapy for chronic myelogenous Leukemia.
- What do kinase inhibition profiles tell us about tyrosine kinase inhibitors used for the treatment of CML?
- The BCR-ABL35INS insertion/truncation mutant is kinase-inactive and does not contribute to tyrosine kinase inhibitor resistance in chronic myeloid Leukemia.
- Advances in the treatment of chronic Myeloid Leukemia.
- TNF? facilitates clonal expansion of JAK2V617F positive Cells in myeloproliferative neoplasms.
- Human chronic myeloid Leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity.
- BCR-ABL SH3-SH2 domain mutations in chronic myeloid Leukemia patients on imatinib.
- Resistance to imatinib: mutations and beyond.
- MET receptor sequence variants R970C and T992I lack transforming capacity.
- CYT387, a novel JAK2 inhibitor, induces hematologic responses and normalizes inflammatory cytokines in murine Myeloproliferative neoplasms.
- How much and how long: tyrosine kinase inhibitor therapy in chronic myeloid Leukemia.
- Acute dasatinib exposure commits Bcr-Abl-dependent cells to apoptosis.
- Same mutation, different allele.
- RNAi screen for rapid therapeutic target identification in Leukemia patients.
- ERK2, but not ERK1, mediates acquired and "de novo" resistance to imatinib mesylate: implication for CML therapy.
- A BCR-ABL mutant lacking direct binding sites for the GRB2, CBL and CRKL adapter proteins fails to induce Leukemia in mice.
- Toward a cure for chronic myeloid Leukemia.
- Absence of SKP2 expression attenuates BCR-ABL-induced Myeloproliferative disease.
- Persistent LYN signaling in imatinib-resistant, BCR-ABL-independent chronic myelogenous Leukemia.
- High-throughput sequence analysis of the tyrosine kinome in Acute myeloid leukemia.
- SGX393 inhibits the CML mutant Bcr-AblT315I and preempts in vitro resistance when combined with nilotinib or dasatinib.
- New strategies for the first-line treatment of chronic myeloid Leukemia: can resistance be avoided?
- RNAi screening of the tyrosine kinome identifies therapeutic targets in Acute myeloid leukemia.
- Chronic myeloid Leukemia: an historical perspective.
- Milestones and monitoring in patients with CML treated with imatinib.
- Identification of driver and passenger mutations of FLT3 by high-throughput DNA sequence analysis and functional assessment of candidate alleles.
- Therapeutic drug monitoring in CML patients on imatinib.
- Bcr-Abl kinase domain mutations and the unsettled problem of Bcr-AblT315I: looking into the future of controlling drug resistance in chronic myeloid Leukemia.
- Antileukemic activity of lysophosphatidic acid acyltransferase-beta inhibitor CT32228 in chronic myelogenous Leukemia sensitive and resistant to imatinib.
- Comparison of imatinib mesylate, dasatinib (BMS-354825), and nilotinib (AMN107) in an N-ethyl-N-nitrosourea (ENU)-based mutagenesis screen: high efficacy of drug combi...
- Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib.
- Activating alleles of JAK3 in Acute megakaryoblastic leukemia.
- BCR-ABL mRNA levels at and after the time of a complete cytogenetic response (CCR) predict the duration of CCR in imatinib mesylate-treated patients with CML.
- High-sensitivity detection of BCR-ABL kinase domain mutations in imatinib-naive patients: correlation with clonal cytogenetic evolution but not response to therapy.
- RNAi-induced down-regulation of FLT3 expression in AML Cell lines increases sensitivity to MLN518.
- Inhibition of wild-type and mutant Bcr-Abl by AP23464, a potent ATP-based oncogenic protein kinase inhibitor: implications for CML.
- In vitro efficacy of combined treatment depends on the underlying mechanism of resistance in imatinib-resistant Bcr-Abl-positive Cell lines.
- SeVeral Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib.
- Activity of the Bcr-Abl kinase inhibitor PD180970 against clinically relevant Bcr-Abl isoforms that cause resistance to imatinib mesylate (Gleevec, STI571).
- A phase 2 study of imatinib in patients with relapsed or refractory Philadelphia chromosome-positive Acute lymphoid leukemias.
- Deletions of the derivative chromosome 9 do not account for the poor prognosis associated with Philadelphia-positive Acute lymphoblastic leukemia.
Procedures Preformed
- HPC Transplantation (Stem Cell Transplant)
- Plasmapheresis
Conditions Treated
- Acute Leukemia
- Anemia
- Chronic Myeloid Leukemia (CML)
- Deep Vein Thrombosis (DVT)
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Doctors Specialties
- Hematology
Accepted Insurances
Hospital
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University of Utah Health Care - Hospital and Clinics
Drug Facts
| NPI NUMBER | 1932115524 | |
| NPPES Provider LastName | DEININGER | |
| NPPES Provider FirstName | MICHAEL | |
| NPPES Provider ZIPCode | 841125500 | |
| NPPES Provider State | UT | |
| Specialty Description | Hematology | |
| Total Claim Count | 151.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1932115524 |
| Last Name Of The Provider | DEININGER |
| First Name Of The Provider | MICHAEL |
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