Professor of Medicine, Oregon Health and Sci University
Hematology
Dr. Brian J. Druker, MD
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Brian Druker works in the field of Hematology. He researched medicine at University of California San Diego School of Medicine. University of California San Diego School of Medicine is ranked 17 in research and 19 in primary care medicine He received awards:"America's Top Doctors", "America's Top Doctors for Cancer", "Portland Monthly Magazine", "Elected Member", "Whos Who in Medicine and Healthcare" and "Investigator". Brian J. Druker, MD is also published. He has 101 publications published. The lastest publication: "Extreme mutational selectivity of axitinib limits its potential use as a targeted therapeutic for BCR-ABL1-positive leukemia.' He accepts Medicare.
Publications
- The NIH BD2K center for big data in translational genomics.
- Extreme mutational selectivity of axitinib limits its potential use as a targeted therapeutic for BCR-ABL1-positive Leukemia.
- Mutant calreticulin-expressing cells induce monocyte hyperreactivity through a paracrine mechanism.
- Self-Enforcing Feedback Activation between BCL6 and Pre-B Cell Receptor Signaling Defines a Distinct Subtype of Acute Lymphoblastic Leukemia.
- Crosstalk between KIT and FGFR3 Promotes Gastrointestinal Stromal Tumor Cell Growth and Drug Resistance.
- BCR-ABL1 promotes Leukemia by converting p27 into a cytoplasmic oncoprotein.
- A therapeutically targetable mechanism of BCR-ABL-independent imatinib resistance in chronic myeloid Leukemia.
- BCR-ABL1 Compound Mutations Combining Key Kinase Domain Positions Confer Clinical Resistance to Ponatinib in Ph Chromosome-Positive Leukemia.
- A potential therapeutic strategy for chronic lymphocytic Leukemia by combining Idelalisib and GS-9973, a novel spleen tyrosine kinase (Syk) inhibitor.
- PDGFRβ reverses EphB4 signaling in alveolar rhabdomyosarcoma.
- Janet Rowley (1925-2013).
- Antagonism of SET using OP449 enhances the efficacy of tyrosine kinase inhibitors and overcomes drug resistance in 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 ...
- Foretinib is a potent inhibitor of oncogenic ROS1 fusion proteins.
- Mouse model of intrahepatic cholangiocarcinoma validates FIG-ROS as a potent fusion oncogene and therapeutic target.
- The CSF3R T618I mutation causes a lethal neutrophilic neoplasia in mice that is responsive to therapeutic JAK inhibition.
- Kinase Inhibitor Therapy in CML: It's What's Inside That Counts.
- Dynamic and Nuclear expression of Pdgfrα and Igf1r in Alveolar Rhabdomyosarcoma.
- The PI3K/Akt1 pathway enhances steady-State levels of FANCL.
- CX-4945, a selective inhibitor of casein kinase 2 (CK2), exhibits anti-tumor activity in hematologic malignancies including enhanced activity in Chronic lymphocytic le...
- 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.
- Threshold levels of ABL tyrosine kinase inhibitors retained in chronic myeloid Leukemia cells define commitment to apoptosis.
- Imatinib and Dasatinib Inhibit Hemangiosarcoma and Implicate PDGFR-? and Src in Tumor Growth.
- HitWalker: variant prioritization for personalized functional Cancer genomics.
- BCR-ABL1 compound mutations in tyrosine kinase inhibitor-resistant CML: frequency and clonal relationships.
- The selective Syk inhibitor P505-15 inhibits B cell signaling and function in vitro and in vivo, and augments the activity of fludarabine in chronic lymphocytic Leukemia.
- Crosstalk between ROR1 and the Pre-B Cell Receptor Promotes Survival of t(1;19) Acute Lymphoblastic Leukemia.
- Imatinib mesylate causes growth deceleration in pediatric patients with chronic myelogenous Leukemia.
- Kinase Pathway Dependence in Primary Human Leukemias Determined by Rapid Inhibitor Screening.
- Effects of plerixafor in combination with BCR-ABL kinase inhibition in a murine model of CML.
- Genomics: the Breast cancer landscape.
- FANCL ubiquitinates beta-catenin and enhances its nuclear function.
- Nilotinib and MEK Inhibitors Induce Synthetic Lethality through Paradoxical Activation of RAF in Drug-Resistant Chronic Myeloid Leukemia.
- In vitro sensitivity to dasatinib in lymphoblasts from a patient with t(17;19)(q22;p13) gene rearrangement pre-B Acute lymphoblastic leukemia.
- Will Imatinib Compromise Reproductive Capacity?
- BCL6-mediated repression of p53 is critical for Leukemia stem cell survival in chronic myeloid Leukemia.
- The BCR-ABL35INS insertion/truncation mutant is kinase-inactive and does not contribute to tyrosine kinase inhibitor resistance in chronic myeloid Leukemia.
- TNF? facilitates clonal expansion of JAK2V617F positive cells in Myeloproliferative neoplasms.
- Multiplex Mutation Screening by Mass Spectrometry: Evaluation of 820 Cases from a Personalized Cancer Medicine Registry.
- The ABL Switch Control Inhibitor DCC-2036 Is Active against the Chronic Myeloid Leukemia Mutant BCR-ABLT315I and Exhibits a Narrow Resistance Profile.
- Potent activity of ponatinib (AP24534) in models of FLT3-driven Acute myeloid leukemia (AML) and other hematologic malignancies.
- Targeting the BCR-ABL signaling pathway in therapy-resistant Philadelphia chromosome-positive Leukemia.
- CAL-101, a p110delta selective phosphatidylinositol-3-kinase inhibitor for the treatment of B-cell Malignancies, inhibits PI3K signaling and cellular viability.
- Human chronic myeloid Leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity.
- Survey of activated FLT3 signaling in Leukemia.
- BCR-ABL SH3-SH2 domain mutations in chronic myeloid Leukemia patients on imatinib.
- A specific need for CRKL in p210BCR-ABL-induced transformation of mouse hematopoietic progenitors.
- MET receptor sequence variants R970C and T992I lack transforming capacity.
- Wnt/Ca2+/NFAT signaling maintains survival of Ph+ Leukemia cells upon inhibition of Bcr-Abl.
- Critical roles for mTORC2- and rapamycin-insensitive mTORC1-complexes in growth and survival of BCR-ABL-expressing leukemic cells.
- CYT387, a novel JAK2 inhibitor, induces hematologic responses and normalizes inflammatory cytokines in murine Myeloproliferative neoplasms.
- Phase III, randomized, open-label study of daily imatinib mesylate 400 mg versus 800 mg in patients with newly diagnosed, previously untreated chronic myeloid Leukemia...
- A gene expression signature of CD34+ cells to predict major cytogenetic response in chronic-phase chronic myeloid Leukemia patients treated with imatinib.
- Preliminary Evidence of Increased Pain and Elevated Cytokines in Fibromyalgia Patients with Defective Growth Hormone Response to Exercise.
- Dasatinib treatment of chronic-phase chronic myeloid Leukemia: analysis of responses according to preexisting BCR-ABL mutations.
- AP24534, a pan-BCR-ABL inhibitor for chronic myeloid Leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance.
- Acute dasatinib exposure commits Bcr-Abl-dependent cells to apoptosis.
- Perspectives on the development of imatinib and the future of Cancer research.
- RNAi screen for therapeutic target in Leukemia.
- Single particle quantum dot imaging achieves ultrasensitive detection capabilities for Western immunoblot analysis.
- RNAi screen for rapid therapeutic target identification in Leukemia patients.
- High-throughput sequencing screen reveals novel, transforming RAS mutations in myeloid Leukemia patients.
- Efficacy of imatinib dose escalation in patients with chronic myeloid Leukemia in chronic phase.
- A BCR-ABL mutant lacking direct binding sites for the GRB2, CBL and CRKL adapter proteins fails to induce Leukemia in mice.
- Translation of the Philadelphia chromosome into therapy for CML.
- Inhibition of polysome assembly enhances imatinib activity against chronic myelogenous Leukemia and overcomes imatinib resistance.
- Absence of SKP2 expression attenuates BCR-ABL-induced myeloproliferative Disease.
- High-throughput sequence analysis of the tyrosine kinome in Acute myeloid leukemia.
- Suppression of interferon (IFN)-inducible genes and IFN-mediated functional responses in BCR-ABL-expressing cells.
- Suppression of programmed cell death 4 (PDCD4) protein expression by BCR-ABL-regulated engagement of the mTOR/p70 S6 kinase pathway.
- An intron-derived insertion/truncation mutation in the BCR-ABL kinase domain in chronic myeloid Leukemia patients undergoing kinase inhibitor therapy.
- RNAi screening of the tyrosine kinome identifies therapeutic targets in Acute myeloid leukemia.
- Inhibition of p38 MAPK suppresses inflammatory cytokine induction by etoposide, 5-fluorouracil, and doxorubicin without affecting tumoricidal activity.
- Growth arrest of BCR-ABL positive cells with a sequence-specific polyamide-chlorambucil conjugate.
- Differential expression of novel tyrosine kinase substrates during Breast cancer development.
- Identification of driver and passenger mutations of FLT3 by high-throughput DNA sequence analysis and functional assessment of candidate alleles.
- Rac guanosine triphosphatases represent integrating molecular therapeutic targets for BCR-ABL-induced myeloproliferative Disease.
- Progressive loss of epidermal growth factor receptor in a subpopulation of Breast cancers: implications in target-directed therapeutics.
- A half-log increase in BCR-ABL RNA predicts a higher risk of relapse in patients with chronic myeloid Leukemia with an imatinib-induced complete cytogenetic response.
- Binding of Cbl to a phospholipase Cgamma1-docking site on platelet-derived growth factor receptor beta provides a dual mechanism of negative regulation.
- The prognosis for patients with chronic myeloid Leukemia who have clonal cytogenetic abnormalities in philadelphia chromosome-negative cells.
- FTY720, a new alternative for treating blast crisis chronic myelogenous leukemia and Philadelphia chromosome-positive Acute lymphocytic leukemia.
- Therapeutic drug monitoring in CML patients on imatinib.
- Applying the discovery of the Philadelphia chromosome.
- A novel fusion of RBM6 to CSF1R in Acute megakaryoblastic leukemia.
- Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid Leukemia after failure of imatinib therapy.
- SHP-2 phosphatase is required for hematopoietic cell transformation by Bcr-Abl.
- Phosphotyrosine profiling identifies the KG-1 cell line as a model for the study of FGFR1 fusions in Acute myeloid leukemia.
- Characterization of murine JAK2V617F-positive myeloproliferative Disease.
- Phase 1 clinical results with tandutinib (MLN518), a novel FLT3 antagonist, in patients with Acute myelogenous leukemia or high-risk myelodysplastic syndrome: safety, ...
- Antileukemic activity of lysophosphatidic acid acyltransferase-beta inhibitor CT32228 in chronic myelogenous Leukemia sensitive and resistant to imatinib.
- Bim and Bad mediate imatinib-induced killing of Bcr/Abl+ leukemic cells, and resistance due to their loss is overcome by a BH3 mimetic.
- 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...
- The Cancer chemotherapy drug etoposide (VP-16) induces proinflammatory cytokine production and sickness behavior-like symptoms in a mouse model of Cancer chemotherapy-...
- Survival advantage from imatinib compared with the combination interferon-alpha plus cytarabine in chronic-phase chronic myelogenous Leukemia: historical comparison be...
- Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib.
- Monitoring CML patients responding to treatment with tyrosine kinase inhibitors: review and recommendations for harmonizing current methodology for detecting BCR-ABL t...
- Activating alleles of JAK3 in Acute megakaryoblastic leukemia.
- Circumventing resistance to kinase-inhibitor therapy.
Schools
University Of California San Diego School Of Medicine
Barnes Jewish Hospital S Campus
Dana Farber Cancer Institute
Conditions Treated
- Acute Leukemia
- Anemia
- Breast Cancer
- Chronic Myeloid Leukemia (CML)
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Doctors Specialties
- Medical Oncology
- Oncology
- Hematology
Accepted Insurances
- Choice Plus POS II
- Blue Card PPO
- Cigna PPO
- Great West Healthcare-Cigna PPO
- Open Access Plus
- Commercial Insurance Company
- First Choice Health PPO
- First Health (Coventry Health Care) PPO
- Health Plan of Oregon PPO
- Medicare Advantage PFFS
- Humana
- Medicare MCR
- ODS Health Plan
- Preferred PSN
- Heritage Plus
- Heritage Signature
- Preferred PPO
- Preferred Provider Network PPN
- Choice Plus POS
- Options PPO
- PacifiCare HMO
- United Healthcare
Awards
- America's Top Doctors
- America's Top Doctors for Cancer
- Portland Monthly Magazine
- Elected Member
- Whos Who in Medicine and Healthcare
- Investigator
Education
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Washington University - Barnes-Jewish Hospital -
University of California San Diego School of Medicine
Drug Facts
| NPI NUMBER | 1528073012 | |
| NPPES Provider LastName | DRUKER | |
| NPPES Provider FirstName | BRIAN | |
| NPPES Provider ZIPCode | 97239 | |
| NPPES Provider State | OR | |
| Specialty Description | Hematology/Oncology | |
| Total Claim Count | 45.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1528073012 |
| Last Name Of The Provider | DRUKER |
| First Name Of The Provider | BRIAN |
| View All |
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