Neil P Shah

Summary

Affiliation: University of California
Country: USA

Publications

  1. doi request reprint Bench to bedside: BRCA: from therapeutic target to therapeutic shield
    Neil P Shah
    Nat Med 14:495-6. 2008
  2. pmc Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop
    Sergei Roumiantsev
    Center for Blood Research and Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115 5717, USA
    Proc Natl Acad Sci U S A 99:10700-5. 2002
  3. ncbi request reprint Structure of the kinase domain of an imatinib-resistant Abl mutant in complex with the Aurora kinase inhibitor VX-680
    Matthew A Young
    Departments of Molecular and Cell Biology and Chemistry, Howard Hughes Medical Institute, The University of California at Berkeley, Berkeley, CA 94720, USA
    Cancer Res 66:1007-14. 2006
  4. ncbi request reprint Dasatinib
    Neil P Shah
    Division of Hematology Oncology, UCSF School of Medicine, San Francisco, California 94143, USA
    Drugs Today (Barc) 43:5-12. 2007
  5. ncbi request reprint Progressive thoughts about progressive disease
    Neil P Shah
    Division of Hematology Oncology, University of California, San Francisco, San Francisco, California 94143, USA
    Clin Cancer Res 13:5229-31. 2007
  6. pmc Differential effects of dosing regimen on the safety and efficacy of dasatinib: retrospective exposure-response analysis of a Phase III study
    Xiaoning Wang
    Discovery Medicine and Clinical Pharmacology, Bristol Myers Squibb, Lawrenceville, NJ, USA
    Clin Pharmacol 5:85-97. 2013
  7. pmc Potent, transient inhibition of BCR-ABL with dasatinib 100 mg daily achieves rapid and durable cytogenetic responses and high transformation-free survival rates in chronic phase chronic myeloid leukemia patients with resistance, suboptimal response or int
    Neil P Shah
    1Division of Hematology and Oncology, University of California, San Francisco School of Medicine, San Francisco, CA, USA
    Haematologica 95:232-40. 2010
  8. doi request reprint Transient potent BCR-ABL inhibition is sufficient to commit chronic myeloid leukemia cells irreversibly to apoptosis
    Neil P Shah
    Division of Hematology Oncology, Department of Medicine, UCSF School of Medicine, San Francisco, CA 94143, USA
    Cancer Cell 14:485-93. 2008
  9. doi request reprint Intermittent target inhibition with dasatinib 100 mg once daily preserves efficacy and improves tolerability in imatinib-resistant and -intolerant chronic-phase chronic myeloid leukemia
    Neil P Shah
    Division of Hematology Oncology, University of California, San Francisco School of Medicine, Box 1270, 505 Parnassus Ave, San Francisco, CA 94143, USA
    J Clin Oncol 26:3204-12. 2008
  10. ncbi request reprint Advanced CML: therapeutic options for patients in accelerated and blast phases
    Neil P Shah
    Division of Hematology Oncology, University of California, San Francisco, San Francisco, California, 94143, USA
    J Natl Compr Canc Netw 6:S31-S36. 2008

Collaborators

Detail Information

Publications31

  1. doi request reprint Bench to bedside: BRCA: from therapeutic target to therapeutic shield
    Neil P Shah
    Nat Med 14:495-6. 2008
  2. pmc Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop
    Sergei Roumiantsev
    Center for Blood Research and Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115 5717, USA
    Proc Natl Acad Sci U S A 99:10700-5. 2002
    ..Because clinical resistance induced by the Y253F mutation might be overcome by dose escalation of STI-571, molecular genotyping of STI-571-resistant patients may provide information useful for rational therapeutic management...
  3. ncbi request reprint Structure of the kinase domain of an imatinib-resistant Abl mutant in complex with the Aurora kinase inhibitor VX-680
    Matthew A Young
    Departments of Molecular and Cell Biology and Chemistry, Howard Hughes Medical Institute, The University of California at Berkeley, Berkeley, CA 94720, USA
    Cancer Res 66:1007-14. 2006
    ....
  4. ncbi request reprint Dasatinib
    Neil P Shah
    Division of Hematology Oncology, UCSF School of Medicine, San Francisco, California 94143, USA
    Drugs Today (Barc) 43:5-12. 2007
    ..S. Food and Drug Administration for the treatment of imatinib-resistant and -intolerant chronic myeloid leukemia as well as its full approval for the treatment of therapy-resistant Ph+ acute lymphoblastic leukemia...
  5. ncbi request reprint Progressive thoughts about progressive disease
    Neil P Shah
    Division of Hematology Oncology, University of California, San Francisco, San Francisco, California 94143, USA
    Clin Cancer Res 13:5229-31. 2007
  6. pmc Differential effects of dosing regimen on the safety and efficacy of dasatinib: retrospective exposure-response analysis of a Phase III study
    Xiaoning Wang
    Discovery Medicine and Clinical Pharmacology, Bristol Myers Squibb, Lawrenceville, NJ, USA
    Clin Pharmacol 5:85-97. 2013
    ..To better understand the superior benefit-risk profile of dasatinib 100 mg once daily, exposure-response was characterized for efficacy (major cytogenetic response) and safety (pleural effusion)...
  7. pmc Potent, transient inhibition of BCR-ABL with dasatinib 100 mg daily achieves rapid and durable cytogenetic responses and high transformation-free survival rates in chronic phase chronic myeloid leukemia patients with resistance, suboptimal response or int
    Neil P Shah
    1Division of Hematology and Oncology, University of California, San Francisco School of Medicine, San Francisco, CA, USA
    Haematologica 95:232-40. 2010
    ..To better assess durability of response to and tolerability of dasatinib, data from a 2-year minimum follow-up for a dose-optimization study in chronic-phase chronic myeloid leukemia are reported here...
  8. doi request reprint Transient potent BCR-ABL inhibition is sufficient to commit chronic myeloid leukemia cells irreversibly to apoptosis
    Neil P Shah
    Division of Hematology Oncology, Department of Medicine, UCSF School of Medicine, San Francisco, CA 94143, USA
    Cancer Cell 14:485-93. 2008
    ..In CML patients receiving dasatinib once daily, response correlates with the magnitude of BCR-ABL kinase inhibition, thereby demonstrating the potential clinical utility of intermittent potent kinase inhibitor therapy...
  9. doi request reprint Intermittent target inhibition with dasatinib 100 mg once daily preserves efficacy and improves tolerability in imatinib-resistant and -intolerant chronic-phase chronic myeloid leukemia
    Neil P Shah
    Division of Hematology Oncology, University of California, San Francisco School of Medicine, Box 1270, 505 Parnassus Ave, San Francisco, CA 94143, USA
    J Clin Oncol 26:3204-12. 2008
    ..Once-daily treatment resulted in less toxicity, suggesting that toxicity results from continuous inhibition of unintended targets. Here, a dose- and schedule-optimization study is reported...
  10. ncbi request reprint Advanced CML: therapeutic options for patients in accelerated and blast phases
    Neil P Shah
    Division of Hematology Oncology, University of California, San Francisco, San Francisco, California, 94143, USA
    J Natl Compr Canc Netw 6:S31-S36. 2008
    ..However, BCR-ABL-independent pathways may also become more important, indicating that other therapeutic targets may also have a future role in managing patients with advanced CML...
  11. pmc Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency
    Neil P Shah
    Division of Hematology Oncology, Department of Medicine, UCSF School of Medicine, San Francisco, California, USA
    J Clin Invest 117:2562-9. 2007
    ....
  12. doi request reprint Dasatinib 140 mg once daily versus 70 mg twice daily in patients with Ph-positive acute lymphoblastic leukemia who failed imatinib: Results from a phase 3 study
    Michael B Lilly
    Chao Family Comprehensive Cancer Center, University of California, Irvine, Orange, USA
    Am J Hematol 85:164-70. 2010
    ..Compared with the 70 mg twice daily, dasatinib 140 mg once daily had similar overall efficacy and safety in patients with imatinib-resistant or intolerant Ph+ ALL. (clinicaltrials.gov identifier: NCT00123487)...
  13. pmc Equally potent inhibition of c-Src and Abl by compounds that recognize inactive kinase conformations
    Markus A Seeliger
    Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkely, USA
    Cancer Res 69:2384-92. 2009
    ..Importantly, several of the DSA compounds block the growth of Ba/F3 cells harboring imatinib-resistant BCR-ABL mutants, including the Thr315Ile "gatekeeper" mutation, but do not suppress the growth of parental Ba/F3 cells...
  14. ncbi request reprint Dasatinib (BMS-354825) inhibits KITD816V, an imatinib-resistant activating mutation that triggers neoplastic growth in most patients with systemic mastocytosis
    Neil P Shah
    Division of Hematology Oncology, The David Geffen School of Medicine at University of California Los Angeles UCLA, CA, USA
    Blood 108:286-91. 2006
    ..Moreover, dasatinib may be of clinical utility in other disease settings driven by activating KIT mutations...
  15. doi request reprint Clonal hematopoiesis in Philadelphia chromosome-negative bone marrow cells of chronic myeloid leukemia patients receiving dasatinib
    Ronald L Paquette
    Department of Medicine, UCLA, 42 121 CHS, Los Angeles, CA, USA
    Leuk Res 34:708-13. 2010
    ..After three years, no patient developed myelodysplastic syndrome or acute myeloid leukemia...
  16. ncbi request reprint Overriding imatinib resistance with a novel ABL kinase inhibitor
    Neil P Shah
    Division of Hematology and Oncology, Department of Medicine, The David Geffen School of Medicine, University of California, Los Angeles, CA, 90095, USA
    Science 305:399-401. 2004
    ..These data illustrate how molecular insight into kinase inhibitor resistance can guide the design of second-generation targeted therapies...
  17. ncbi request reprint Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia
    Neil P Shah
    Department of Medicine, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
    Cancer Cell 2:117-25. 2002
    ..Multiple independent mutant clones were detected in a subset of relapsed cases. Our data support a clonal selection model of preexisting BCR-ABL mutations that confer imatinib resistance...
  18. pmc BCL6-mediated repression of p53 is critical for leukemia stem cell survival in chronic myeloid leukemia
    Christian Hurtz
    Department of Laboratory Medicine, University of California San Francisco, CA 94143, USA
    J Exp Med 208:2163-74. 2011
    ..Clinical validation of this concept could limit the duration of TKI treatment in CML patients, which is currently life-long, and substantially decrease the risk of blast crisis transformation...
  19. pmc Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD
    Catherine C Smith
    Division of Hematology Oncology, University of California, San Francisco, CA, USA
    Blood 121:3165-71. 2013
    ..Alternative strategies will be required for patients with TKI-resistant FLT3-ITD D835 mutations...
  20. doi request reprint Tyrosine kinase inhibitor therapy for chronic myeloid leukemia: approach to patients with treatment-naive or refractory chronic-phase disease
    Catherine C Smith
    Department of Hematology Oncology, University of California San Francisco, San Francisco, CA 94143 1270, USA
    Hematology Am Soc Hematol Educ Program 2011:121-7. 2011
    ..To this end, the latest seminal clinical trial results of approved and investigational BCR-ABL TKIs and some of the salient unique features of each of these agents are summarized herein...
  21. doi request reprint Frequent EVI1 translocations in myeloid blast crisis CML that evolves through tyrosine kinase inhibitors
    Ronald L Paquette
    UCLA Department of Medicine, Los Angeles, CA, USA
    Cancer Genet 204:392-7. 2011
    ..Inhibition of c-ABL kinase-mediated DNA double-strand repair by TKIs may predispose to EVI1 translocation in this setting...
  22. doi request reprint Is it downhill from here? Eliminating leukemic stem cells and curing chronic myeloid leukemia
    Catherine C Smith
    Division of Hematology Oncology, Department of Medicine, University of California at San Francisco, San Francisco, California 94143, USA
    Clin Cancer Res 17:6605-7. 2011
    ..The rate of β decrease is consistent with declining leukemic stem cells and may predict which patients may safely discontinue therapy...
  23. pmc Comparative analysis of two clinically active BCR-ABL kinase inhibitors reveals the role of conformation-specific binding in resistance
    Michael R Burgess
    Molecular Biology Institute, Howard Hughes Medical Institute, and Division of Hematology and Oncology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
    Proc Natl Acad Sci U S A 102:3395-400. 2005
    ..The combination of imatinib plus BMS-354825 greatly reduced the recovery of drug-resistant clones. Our findings provide further rationale for considering kinase conformation in the design of kinase inhibitors against cancer targets...
  24. ncbi request reprint Mechanisms of resistance to STI571 in Philadelphia chromosome-associated leukemias
    Neil P Shah
    Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA
    Oncogene 22:7389-95. 2003
    ..Additionally, genomic amplification of the BCR-ABL gene can occasionally be detected. This review will highlight mechanisms of STI571 resistance in clinical samples as well as preclinical models...
  25. pmc Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia
    Catherine C Smith
    Division of Hematology Oncology, University of California, San Francisco, California 94143, USA
    Nature 485:260-3. 2012
    ..Our findings demonstrate that FLT3-ITD can represent a driver lesion and valid therapeutic target in human AML. AC220-resistant FLT3 kinase domain mutants represent high-value targets for future FLT3 inhibitor development efforts...
  26. doi request reprint The role of kinase inhibitors in the treatment of patients with acute myeloid leukemia
    Catherine C Smith
    From the Division of Hematology Oncology, Department of Medicine, University of California, San Francisco, San Francisco, CA Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA
    Am Soc Clin Oncol Educ Book 33:313-8. 2013
    ....
  27. pmc Inhibition of drug-resistant mutants of ABL, KIT, and EGF receptor kinases
    Todd A Carter
    Ambit, Inc, 4215 Sorrento Valley Boulevard, San Diego, CA 92121, USA
    Proc Natl Acad Sci U S A 102:11011-6. 2005
    ....
  28. ncbi request reprint Detection of BCR-ABL kinase mutations in CD34+ cells from chronic myelogenous leukemia patients in complete cytogenetic remission on imatinib mesylate treatment
    Su Chu
    Division of Hematology and Hematopoietic Cell Transplantation, City of Hope National Medical Center, Duarte, CA 91010, USA
    Blood 105:2093-8. 2005
    ..We conclude that BCR-ABL kinase mutations can be detected in CD34+ cells from CML patients in CCR on imatinib, may contribute to persistence of small populations of malignant progenitors, and could be a potential source of relapse...
  29. ncbi request reprint Dynamics of chronic myeloid leukaemia
    Franziska Michor
    Program for Evolutionary Dynamics, Department of Organismic and Evolutionary Biology, Department of Mathematics, Harvard University, Cambridge, Massachusetts 02138, USA
    Nature 435:1267-70. 2005
    ..We calculate the probability of developing imatinib resistance mutations and estimate the time until detection of resistance. Our model provides the first quantitative insights into the in vivo kinetics of a human cancer...
  30. ncbi request reprint Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy
    Andreas Hochhaus
    III Medizinische Klinik, Medizinische Fakultat Mannheim, Universitat Heidelberg, Theodor Kutzer Ufer 1 3, 68167 Mannheim, Germany
    Blood 109:2303-9. 2007
    ..This trial was registered at www.clinicaltrials.gov as CA180013...
  31. ncbi request reprint Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias
    Moshe Talpaz
    Department of Leukemia, M D Anderson Cancer Center, Houston, USA
    N Engl J Med 354:2531-41. 2006
    ..We evaluated dasatinib, a BCR-ABL inhibitor that targets most imatinib-resistant BCR-ABL mutations, in patients with chronic myelogenous leukemia (CML) or Ph-positive acute lymphoblastic leukemia (ALL)...