Research Topics
Species | Charles SawyersSummaryAffiliation: University of California Country: USA Publications
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Publications
Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II studyCharles L Sawyers
Department of Medicine and Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA
Blood 99:3530-9. 2002..Additional clinical studies are warranted to explore the efficacy and feasibility of imatinib used in combination with other antileukemic drugs...- Finding the next Gleevec: FLT3 targeted kinase inhibitor therapy for acute myeloid leukemiaCharles L Sawyers
Department of Medicine, Molecular Biology Institute, David Geffen School of Medicine, University of California, Los Angeles 90095, USA
Cancer Cell 1:413-5. 2002..Activating mutations in the FLT3 receptor tyrosine kinase occur in 30% of patients with acute myeloid leukemia. Small molecule FLT3 kinase inhibitors show selective antitumor activity in preclinical models. Clinical studies are underway... - Will mTOR inhibitors make it as cancer drugs?Charles L Sawyers
Howard Hughes Medical Institute, Los Angeles, CA 90095, USA
Cancer Cell 4:343-8. 2003 - Opportunities and challenges in the development of kinase inhibitor therapy for cancerCharles L Sawyers
Howard Hughes Medical Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
Genes Dev 17:2998-3010. 2003 - Disabling Abl-perspectives on Abl kinase regulation and cancer therapeuticsCharles L Sawyers
Department of Medicine, Molecular Biology Institute, UCLA School of Medicine, 90095, USA
Cancer Cell 1:13-5. 2002..New findings about Abl kinase domain regulation provide insight into novel strategies for targeted therapy... - Overview: the art of cancer drug screening: molecular target versus milieu-based screensCharles L Sawyers
Department of Hematology/Oncology, University of California, Los Angeles 90095, USA
Curr Opin Investig Drugs 3:478-81. 2002 - Targeted cancer therapyCharles Sawyers
Howard Hughes Medical Institute, David Geffen School of Medicine at UCLA, Jonsson Comprehensive Cancer Center, 10833 LeConte Avenue, Los Angeles, California 90095, USA
Nature 432:294-7. 2004..Recent progress in understanding the molecular changes that underlie cancer development offer the prospect of specifically targeting malfunctioning molecules and pathways to achieve more effective and rational cancer therapy... - BCR-ABL point mutants isolated from patients with imatinib mesylate-resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90Mercedes E Gorre
Department of Medicine and Molecular Biology Institute, David Geffen School of Medicine at University of California, Los Angeles, CA 900095 1678, USA
Blood 100:3041-4. 2002..These data support clinical investigations of 17-AAG in imatinib mesylate-resistant Ph(+) leukemias... - Rational therapeutic intervention in cancer: kinases as drug targetsCharles L Sawyers
11 934 Factor Building, University of California, Los Angeles Division of Hematology and Oncology, 10833 Le Conte Avenue, Los Angeles, California 90095 1678, USA
Curr Opin Genet Dev 12:111-5. 2002..These examples have galvanized the cancer research community to extend kinase-inhibitor therapy to other cancers... - Molecular abnormalities in myeloid leukemias and myelodysplastic syndromesC L Sawyers
Department of Medicine, University of California, Los Angeles 90095 1678, USA
Leuk Res 22:1113-22. 1998..Recent insights into the molecular basis of these leukemias is presented using selected examples from these groups... 
Frequent EVI1 translocations in myeloid blast crisis CML that evolves through tyrosine kinase inhibitorsRonald 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...
Evidence for regulation of the PTEN tumor suppressor by a membrane-localized multi-PDZ domain containing scaffold protein MAGI-2X Wu
Department of Medicine, Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA
Proc Natl Acad Sci U S A 97:4233-8. 2000..We propose that MAGI-2 improves the efficiency of PTEN signaling through assembly of a multiprotein complex at the cell membrane...- c-Abl is required for development and optimal cell proliferation in the context of p53 deficiencyY E Whang
Department of Medicine, University of California, Los Angeles, CA 90095, USA
Proc Natl Acad Sci U S A 97:5486-91. 2000..Inhibition of c-Abl function may be a therapeutic strategy to target p53-deficient cells selectively... - Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplificationM E Gorre
Department of Medicine, Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA
Science 293:876-80. 2001..These studies provide evidence that genetically complex cancers retain dependence on an initial oncogenic event and suggest a strategy for identifying inhibitors of STI-571 resistance... - Enhanced sensitivity of PTEN-deficient tumors to inhibition of FRAP/mTORM S Neshat
Department of Medicine, University of California School of Medicine, Los Angeles, CA 90095, USA
Proc Natl Acad Sci U S A 98:10314-9. 2001..These results provide rationale for testing FRAP/mTOR inhibitors in PTEN null human cancers... - Monitoring antiproliferative responses to kinase inhibitor therapy in mice with 3'-deoxy-3'-18F-fluorothymidine PETChristian Waldherr
Department of Molecular and Medical Pharmacology, Ahmanson Biological Imaging Center, David Geffen School of Medicine, University of California at Los Angeles, 10833 Le Conte Ave, Los Angeles, CA 90095, USA
J Nucl Med 46:114-20. 2005.... - Dynamics of chronic myeloid leukaemiaFranziska 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... - Inhibition of drug-resistant mutants of ABL, KIT, and EGF receptor kinasesTodd A Carter
Ambit, Inc, 4215 Sorrento Valley Boulevard, San Diego, CA 92121, USA
Proc Natl Acad Sci U S A 102:11011-6. 2005.... - Calculated resistance in cancerCharles L Sawyers
Nat Med 11:824-5. 2005 - Update on the use of imatinib mesylateCharles L Sawyers
University of California, Los Angeles, 90095, USA
Clin Adv Hematol Oncol 3:757-8. 2005 - Hypoxia-inducible factor determines sensitivity to inhibitors of mTOR in kidney cancerGeorge V Thomas
Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
Nat Med 12:122-7. 2006..Our findings provide preclinical rationale for prospective, biomarker-driven clinical studies of mTOR inhibitors in kidney cancer and suggest that FDG-PET scans may have use as a pharmacodynamic marker in this setting... - Antibody-based profiling of the phosphoinositide 3-kinase pathway in clinical prostate cancerGeorge V Thomas
Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, California 90095, USA
Clin Cancer Res 10:8351-6. 2004..These three antibodies are potentially able to define a molecular signature of PTEN loss and/or AKT pathway activation in prostate cancer... - HER2/neu kinase-dependent modulation of androgen receptor function through effects on DNA binding and stabilityIngo K Mellinghoff
Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
Cancer Cell 6:517-27. 2004..Surprisingly, the downstream signaling pathway responsible for these effects appears to involve kinases other than Akt. These data suggest that the HER2/ERBB3 pathway is a critical target in hormone-refractory prostate cancer... - Structure of the kinase domain of an imatinib-resistant Abl mutant in complex with the Aurora kinase inhibitor VX-680Matthew 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.... - IkappaB kinase beta inhibition induces cell death in Imatinib-resistant and T315I Dasatinib-resistant BCR-ABL+ cellsElizabeth A Duncan
Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599 7295, USA
Mol Cancer Ther 7:391-7. 2008..These data indicate that blockage of BCR-ABL-induced NF-kappaB activation via IkappaB kinase beta inhibition represents a potential new approach for treatment of Imatinib- or Dasatinib-resistant forms of chronic myelogenous leukemia... - Antitumor activity of rapamycin in a Phase I trial for patients with recurrent PTEN-deficient glioblastomaTim F Cloughesy
Department of Neurology, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America
PLoS Med 5:e8. 2008..Small, molecularly focused clinical studies offer the promise of the early definition of optimal biologic dose and patient population... - Cancer: mixing cocktailsCharles L Sawyers
Nature 449:993-6. 2007 - Where lies the blame for resistance--tumor or host?Charles L Sawyers
Nat Med 13:1144-5. 2007 - Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potencyNeil P Shah
Division of Hematology Oncology, Department of Medicine, UCSF School of Medicine, San Francisco, California, USA
J Clin Invest 117:2562-9. 2007.... 
Epidermal growth factor receptor activation in glioblastoma through novel missense mutations in the extracellular domainJeffrey C Lee
Department of Medical Oncology and Center for Cancer Genome Discovery, Dana Farber Cancer Institute Harvard Medical School, Boston, Massachusetts, United States of America
PLoS Med 3:e485. 2006..Missense mutations in the EGFR kinase domain, for example, have recently been identified in patients who showed clinical responses to EGFR kinase inhibitor therapy...- Phosphorylation of the ATP-binding loop directs oncogenicity of drug-resistant BCR-ABL mutantsBrian J Skaggs
Howard Hughes Medical Institute, University of California, Los Angeles, CA 90095, USA
Proc Natl Acad Sci U S A 103:19466-71. 2006..Therefore, mutations that confer clinical resistance to kinase inhibitors can substantially alter kinase function and confer novel biological properties that may impact disease progression... - Mammalian target of rapamycin inhibition promotes response to epidermal growth factor receptor kinase inhibitors in PTEN-deficient and PTEN-intact glioblastoma cellsMaria Y Wang
Department of Pathology and Laboratory Medicine, Henry E Singleton Brain Tumor Program, Howard Hughes Medical Institute, David Geffen School of Medicine, University of California at Los Angeles, CA 90095 1732, USA
Cancer Res 66:7864-9. 2006..These studies provide strong rationale for combined mTOR/EGFR kinase inhibitor therapy in glioblastoma patients, particularly those with PTEN-deficient tumors... - Treating imatinib-resistant leukemia: the next generation targeted therapiesMichael R Burgess
Molecular Biology Institute, Department of Medicine, The David Geffen School of Medicine, University of California, Los Angeles, USA
ScientificWorldJournal 6:918-30. 2006..This review focuses on the mechanisms of imatinib resistance and the strategies currently being developed to overcome clinical resistance... - Will kinase inhibitors have a dark side?Charles L Sawyers
Department of Medicine, University of California, Los Angeles, Los Angeles, USA
N Engl J Med 355:313-5. 2006 - Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemiasMoshe Talpaz
Department of Leukemia, M.D. Anderson Cancer Center, Houston, USA
N Engl J Med 354:2531-41. 2006..CONCLUSIONS: Dasatinib induces hematologic and cytogenetic responses in patients with CML or Ph-positive ALL who cannot tolerate or are resistant to imatinib. (ClinicalTrials.gov number, NCT00064233 [ClinicalTrials.gov].)... - Detection of BCR-ABL kinase mutations in CD34+ cells from chronic myelogenous leukemia patients in complete cytogenetic remission on imatinib mesylate treatmentSu 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... - Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CMLCatriona H M Jamieson
Division of Hematology, Stanford University School of Medicine, Stanford, Calif 94305-5323, USA
N Engl J Med 351:657-67. 2004..CONCLUSIONS: Activation of beta-catenin in CML granulocyte-macrophage progenitors appears to enhance the self-renewal activity and leukemic potential of these cells... - Molecular mechanisms of resistance to STI571 in chronic myeloid leukemiaMercedes E Gorre
Department of Medicine and Molecular Biology Institute, University of California, Los Angeles, California 90095-1678, USA
Curr Opin Hematol 9:303-7. 2002..Here the authors review recent work aimed at elucidating the nature of STI51 resistance... - A novel pyridopyrimidine inhibitor of abl kinase is a picomolar inhibitor of Bcr-abl-driven K562 cells and is effective against STI571-resistant Bcr-abl mutantsDavid R Huron
Department of Medicine, Memorial Sloan-Kettering Cancer Center and Program in Pharmacology, New York, New York 10021, USA
Clin Cancer Res 9:1267-73. 2003..PD166326 is a prototype of a new generation of anti-Bcr-abl compounds with picomolar potency and substantial activity against STI571-resistant mutants... - Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatmentRavi Bhatia
Division of Hematology and Bone Marrow Transplantation, City of Hope National Medical Center, Duarte, CA 91010, USA
Blood 101:4701-7. 2003..Patients in CCR with imatinib mesylate treatment need to be followed carefully to assess for risk of relapse... - Hematopathologic and cytogenetic findings in imatinib mesylate-treated chronic myelogenous leukemia patients: 14 months' experienceRita M Braziel
Dept of Pathology, Oregon Health Sciences University, Portland, OR 97201, USA
Blood 100:435-41. 2002..Several patients acquired additional clonal cytogenetic abnormalities during therapy, a finding with significant implications for prognosis and laboratory monitoring in imatinib mesylate-treated CML patients... - The emergence of resistance to targeted cancer therapeuticsIngo K Mellinghoff
Departments of Medicine and Molecular Biology Institute, UCLA School of Medicine, Los Angeles, CA 90095, USA
Pharmacogenomics 3:603-23. 2002..This article reviews the mechanisms of drug resistance to a variety of cancer therapeutics and provides an approach for how measures of drug target activity can be incorporated into clinical trial design... - Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemiaNeil 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... - Imatinib GIST keeps finding new indications: successful treatment of dermatofibrosarcoma protuberans by targeted inhibition of the platelet-derived growth factor receptorCharles L Sawyers
J Clin Oncol 20:3568-9. 2002 - A phase 2 study of imatinib in patients with relapsed or refractory Philadelphia chromosome-positive acute lymphoid leukemiasOliver G Ottmann
Medizinische Klinik III Abteilung Haematologie, Johann Wolfgang Goethe Universitat, 60590 Frankfurt, Germany
Blood 100:1965-71. 2002..Further studies are warranted to test the effects of imatinib in combination with other agents and to define the mechanisms of resistance to imatinib... - Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loopSergei 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... - Analysis of the phosphatidylinositol 3'-kinase signaling pathway in glioblastoma patients in vivoGheeyoung Choe
Departments of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095, USA
Cancer Res 63:2742-6. 2003..These results provide the first dissection of the PI3K pathway in glioblastoma in vivo and suggest an approach to stratifying patients for targeted kinase inhibitor therapy... - Imatinib mesylate (STI571) inhibits growth of primitive malignant progenitors in chronic myelogenous leukemia through reversal of abnormally increased proliferationMelissa S Holtz
Division of Hematology and Bone Marrow Transplantation and the Department of Cytogenetics, City of Hope National Medical Center, Duarte, CA 91010, USA
Blood 99:3792-800. 2002..These results suggest that inhibition of Bcr-Abl tyrosine kinase by imatinib mesylate restores normal hematopoiesis by removing the proliferative advantage of CML progenitors but that elimination of all CML progenitors may not occur... - Myc-driven murine prostate cancer shares molecular features with human prostate tumorsKatharine Ellwood-Yen
Department of Medicine, and Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
Cancer Cell 4:223-38. 2003..This approach illustrates how genomic technologies can be applied to mouse cancer models to guide evaluation of human tumor databases... - Overriding imatinib resistance with a novel ABL kinase inhibitorNeil 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... - TORward AKTually useful mouse modelsIngo K Mellinghoff
Nat Med 10:579-80. 2004 - Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia: results of a phase 2 studyMoshe Talpaz
M D Anderson Cancer Center, Houston, Texas, USA
Blood 99:1928-37. 2002..Orally administered imatinib is an effective and well-tolerated treatment for patients with CML in accelerated phase. A daily dose of 600 mg is more effective than 400 mg, with similar toxicity... - Mechanisms of resistance to STI571 in Philadelphia chromosome-associated leukemiasNeil 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... - AKT activity determines sensitivity to mammalian target of rapamycin (mTOR) inhibitors by regulating cyclin D1 and c-myc expressionJoseph F Gera
Department of Medicine, West Los Angeles Veteran s Administration UCLA Medical Center, University of California School of Medicine, Los Angeles, California 90073, USA
J Biol Chem 279:2737-46. 2004..These results identify two critical downstream molecular targets whose expression is regulated by AKT activity and whose down-regulation is required for rapamycin/CCI-779 sensitivity... - The phosphatidylinositol 3-Kinase AKT pathway in human cancerIgor Vivanco
Department of Medicine and Molecular Biology Institute, UCLA School of Medicine, 11-935 Factor Building, 10833 LeConte Avenue, Los Angeles, California 90095, USA
Nat Rev Cancer 2:489-501. 2002 - NF-kappa B activates prostate-specific antigen expression and is upregulated in androgen-independent prostate cancerCharlie D Chen
Division of Hematology Oncology, Department of Medicine, University of California at Los Angeles, Los Angeles, California 90095 1678, USA
Mol Cell Biol 22:2862-70. 2002..These results suggest a role of NF-kappa B in prostate cancer progression... - Nineteenth Annual Pezcoller Symposium: hypothesis-driven clinical investigation in cancerWilliam G Kaelin
Dana Farber Cancer Institute, Boston, Massachusetts, USA
Cancer Res 67:11102-5. 2007..A session was devoted to the identification of markers of drug effectiveness. Two sessions were focused on opportunities for developing new specific molecular target-oriented therapies... - The cancer biomarker problemCharles L Sawyers
Howard Hughes Medical Institute, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA
Nature 452:548-52. 2008..One of the main barriers to further progress is identifying the biological indicators, or biomarkers, of cancer that predict who will benefit from a particular targeted therapy... - A prostatic intraepithelial neoplasia-dependent p27 Kip1 checkpoint induces senescence and inhibits cell proliferation and cancer progressionPradip K Majumder
Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
Cancer Cell 14:146-55. 2008..These data suggest that a p27(Kip1)-driven checkpoint limits progression of PIN to CaP... - Growth inhibitory effects of the dual ErbB1/ErbB2 tyrosine kinase inhibitor PKI-166 on human prostate cancer xenograftsIngo K Mellinghoff
Department of Medicine, School of Medicine, University of California-Los Angeles, Los Angeles, CA 90095, USA
Cancer Res 62:5254-9. 2002..These results suggest that ErbB1/ErbB2 RTKs play an important role in the biology of androgen-independent prostate cancer and provide a rationale for clinical evaluation of inhibitors targeted to this pathway... - Molecular determinants of the response of glioblastomas to EGFR kinase inhibitorsIngo K Mellinghoff
Department of Molecular and Medical Pharmacology and Medicine, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles 90095-1732, USA
N Engl J Med 353:2012-24. 2005..In vitro, coexpression of EGFRvIII and PTEN sensitized glioblastoma cells to erlotinib. CONCLUSIONS: Coexpression of EGFRvIII and PTEN by glioblastoma cells is associated with responsiveness to EGFR kinase inhibitors... - Amplification and overexpression of prosaposin in prostate cancerShahriar Koochekpour
Department of Microbiology, Immunology, and Parasitology, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA
Genes Chromosomes Cancer 44:351-64. 2005.... - Transcriptional regulation of a metastasis suppressor gene by Tip60 and beta-catenin complexesJung Hwa Kim
Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 151 742, South Korea
Nature 434:921-6. 2005.... - Comparative analysis of two clinically active BCR-ABL kinase inhibitors reveals the role of conformation-specific binding in resistanceMichael 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... - Molecular determinants of resistance to antiandrogen therapyCharlie D Chen
Department of Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA
Nat Med 10:33-9. 2004..These findings provide insight toward the design of new antiandrogens... - Cross-species comparisons of cancer signalingThomas G Graeber
Nat Genet 37:7-8. 2005 - Pharmacokinetics and pharmacodynamics of imatinib in a phase I trial with chronic myeloid leukemia patientsBin Peng
Clinical Pharmacology, Novartis, One Health Plaza, Building 419, Room 2368, East Hanover, NJ 07936 1080, USA
J Clin Oncol 22:935-42. 2004..To evaluate the basic pharmacokinetic (PK) characteristics of imatinib mesylate and assess the relationship between the PK and pharmacodynamic (PD) properties of the drug... - Context-dependent hormone-refractory progression revealed through characterization of a novel murine prostate cancer cell linePhilip A Watson
Division of Hematology/Oncology, Department of Medicine, University of California at Los Angeles, 90095, USA
Cancer Res 65:11565-71. 2005....