Research Topics
| J G ChristensenSummaryAffiliation: Pfizer Global Research and Development Country: USA Publications
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Detail Information
Publications
In vivo antitumor activity of SU11248, a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor and platelet-derived growth factor receptors: determination of a pharmacokinetic/pharmacodynamic relationshipDirk B Mendel
Preclinical Research and Exploratory Development, SUGEN, Inc, South San Francisco, California 94080, USA
Clin Cancer Res 9:327-37. 2003..The pharmacokinetic/pharmacodynamic relationship established for SU11248 in these preclinical studies has aided in the design, selection, and evaluation of dosing regimens being tested in human trials...- An orally available small-molecule inhibitor of c-Met, PF-2341066, exhibits cytoreductive antitumor efficacy through antiproliferative and antiangiogenic mechanismsHelen Y Zou
Departments of Cancer Biology, Pfizer Global Research and Development, La Jolla Laboratories, La Jolla, California 92121, USA
Cancer Res 67:4408-17. 2007..Collectively, these results show the therapeutic potential of targeting c-Met with selective small-molecule inhibitors for the treatment of human cancers... - A preclinical review of sunitinib, a multitargeted receptor tyrosine kinase inhibitor with anti-angiogenic and antitumour activitiesJ G Christensen
Pfizer Global Research and Development, 10724 Science Center Drive, San Diego, CA 92121, USA
Ann Oncol 18:x3-10. 2007..It also highlights the importance of the multiple pathways that may be involved in cancer progression and the importance of these pathways in selected malignancies... - Pharmacokinetic-pharmacodynamic modeling of biomarker response and tumor growth inhibition to an orally available cMet kinase inhibitor in human tumor xenograft mouse modelsShinji Yamazaki
Pharmacokinetics, Dynamics and Metabolism, La Jolla Laboratories, Pfizer Global Research and Development, 10777 Science Center Dr, San Diego, CA 92121, USA
Drug Metab Dispos 36:1267-74. 2008..The present results will be helpful in determining the appropriate dosing regimen and in guiding dose escalation to rapidly achieve efficacious systemic exposure in the clinic... - PHA665752, a small-molecule inhibitor of c-Met, inhibits hepatocyte growth factor-stimulated migration and proliferation of c-Met-positive neuroblastoma cellsHal E Crosswell
Division of Pediatric Hematology Oncology, Children s Hospital and University Medical Group of the Greenville Hospital System, Greenville, SC 29605, USA
BMC Cancer 9:411. 2009..The effect of the tumor suppressor protein PTEN on migration and proliferation of tumor cells treated with PHA665752 was also evaluated... - Efficacy of c-Met inhibitor for advanced prostate cancerWilliam H Tu
Department of Urology, Stanford University School of Medicine, Stanford, CA 94305 5328, USA
BMC Cancer 10:556. 2010..Therefore, we directly assessed the efficacy of c-Met inhibition during androgen ablation on the growth and progression of prostate cancer... - Beyond VEGF: targeting tumor growth and angiogenesis via alternative mechanismsJames Christensen
Department of Cancer Biology, Pfizer Global Research and Development, La Jolla Laboratories, La Jolla, CA 92121, USA
Adv Exp Med Biol 610:43-53. 2008 - Cytoreductive antitumor activity of PF-2341066, a novel inhibitor of anaplastic lymphoma kinase and c-Met, in experimental models of anaplastic large-cell lymphomaJames G Christensen
Department of Cancer Biology, Pfizer Global Research and Development, La Jolla Laboratories, 10724 Science Center Drive, La Jolla, CA 92121, USA
Mol Cancer Ther 6:3314-22. 2007..Collectively, these data illustrate the potential clinical utility of inhibitors of NPM-ALK in treatment of patients with ALK-positive ALCL... - Plasma vascular endothelial growth factor and interleukin-8 as biomarkers of antitumor efficacy of a prototypical erbB family tyrosine kinase inhibitorJames G Christensen
Pfizer Global Research and Development, La Jolla Labs, CA 92121, USA
Mol Cancer Ther 4:938-47. 2005.... - c-Met as a target for human cancer and characterization of inhibitors for therapeutic interventionJames G Christensen
Research Pharmacology, Pfizer Inc, La Jolla, CA 92121, USA
Cancer Lett 225:1-26. 2005..This review will address the potential for development of c-Met inhibitors for treatment of human cancers with particular emphasis on recent findings with small-molecule inhibitors... - A selective small molecule inhibitor of c-Met kinase inhibits c-Met-dependent phenotypes in vitro and exhibits cytoreductive antitumor activity in vivoJames G Christensen
Preclinical Research and Exploratory Development, SUGEN, Inc, South San Francisco, CA 94080, USA
Cancer Res 63:7345-55. 2003..Collectively, these results demonstrate the feasibility of selectively targeting c-Met with ATP-competitive small-molecules and suggest the therapeutic potential of targeting c-Met in human cancers... - PF-03732010: a fully human monoclonal antibody against P-cadherin with antitumor and antimetastatic activityCathy C Zhang
Translational Research Group in Oncology Research Unit, Pfizer Global Research and Development, La Jolla Laboratories, San Diego, California 92121, USA
Clin Cancer Res 16:5177-88. 2010..We characterized the biological properties of PF-03732010, a human monoclonal antibody against P-cadherin, in cell-based assays and tumor models... - Small-molecule p21-activated kinase inhibitor PF-3758309 is a potent inhibitor of oncogenic signaling and tumor growthBrion W Murray
Pfizer Oncology, Pfizer, San Diego, CA 92121, USA
Proc Natl Acad Sci U S A 107:9446-51. 2010.... - PF-00477736 mediates checkpoint kinase 1 signaling pathway and potentiates docetaxel-induced efficacy in xenograftsCathy Zhang
Oncology Research Unit, Pfizer Global Research and Development, La Jolla Laboratories, San Diego, California, USA
Clin Cancer Res 15:4630-40. 2009..Specifically, we investigated the correlation between PF-00477736-mediated modulation of biomarkers and the sensitization of docetaxel efficacy... - High levels of HER-2 expression alter the ability of epidermal growth factor receptor (EGFR) family tyrosine kinase inhibitors to inhibit EGFR phosphorylation in vivoJ G Christensen
SUGEN, Inc, 230 East Grand Avenue, South San Francisco, CA 94080, USA
Clin Cancer Res 7:4230-8. 2001..The potential clinical implications of this observation are discussed... - Enzymatic characterization of c-Met receptor tyrosine kinase oncogenic mutants and kinetic studies with aminopyridine and triazolopyrazine inhibitorsSergei L Timofeevski
Pfizer Global Research and Development, La Jolla, Pfizer Inc, 10777 Science Center Drive, San Diego, California 92121, USA
Biochemistry 48:5339-49. 2009.... - Multiple circulating proangiogenic factors induced by sunitinib malate are tumor-independent and correlate with antitumor efficacyJohn M L Ebos
Sunnybrook Health Sciences Centre, Molecular and Cellular Biology Research, 2075 Bayview Avenue, Toronto, Ontario, Canada
Proc Natl Acad Sci U S A 104:17069-74. 2007..They may also be relevant to drug-associated toxicities, drug resistance, and observed rapid tumor (re)growth seen after cessation of therapy... - Functional expression and mutations of c-Met and its therapeutic inhibition with SU11274 and small interfering RNA in non-small cell lung cancerPatrick C Ma
Section of Hematology/Oncology, Department of Medicine, University of Chicago Medical Center, Pritzker School of Medicine, Chicago, Illinois, USA
Cancer Res 65:1479-88. 2005..These results indicate that c-Met inhibition will be an important therapeutic strategy against NSCLC to improve its clinical outcome... - Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752Gromoslaw A Smolen
Cancer Center and Department of Pathology, Molecular Pathology Research Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
Proc Natl Acad Sci U S A 103:2316-21. 2006..MET amplification may thus identify a subset of epithelial cancers that are uniquely sensitive to disruption of this pathway and define a patient group that is appropriate for clinical trials of targeted therapy using MET inhibitors... - Sunitinib malate for the treatment of solid tumours: a review of current clinical dataRobert J Motzer
Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
Expert Opin Investig Drugs 15:553-61. 2006..Sunitinib has also demonstrated promising clinical activity in the treatment of other advanced solid tumours. The present review provides an updated summary of emerging clinical experience with this promising new anticancer agent... - Inhibition of c-Met as a therapeutic strategy for esophageal adenocarcinomaGregory A Watson
Department of Surgery, University of Pittsburgh, Pittsburgh, PA, USA
Neoplasia 8:949-55. 2006..Factors other than receptor overexpression, such as c-Met-dependent PI3K/Akt signaling, may be predictive of an individual tumor's response to c-Met inhibition... - A novel small molecule met inhibitor induces apoptosis in cells transformed by the oncogenic TPR-MET tyrosine kinaseMartin Sattler
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Cancer Res 63:5462-9. 2003..The characterization of SU11274 as an effective inhibitor of Met tyrosine kinase activity illustrates the potential of targeting for Met therapeutic use in cancers associated with activated forms of this kinase... - Genomic alterations of anaplastic lymphoma kinase may sensitize tumors to anaplastic lymphoma kinase inhibitorsUltan McDermott
Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, MA 02129, USA
Cancer Res 68:3389-95. 2008..These findings suggest that a subset of lung cancers, lymphomas, and neuroblastomas that harbor genomic ALK alterations may be clinically responsive to pharmacologic ALK inhibition... - An in vivo model of Met-driven lymphoma as a tool to explore the therapeutic potential of Met inhibitorsPaolo Accornero
Department of Anatomy, Pharmacology, and Forensic Medicine, University of Torino, Torino, Italy
Clin Cancer Res 14:2220-6. 2008..A far superior model would be a transgenic line developing spontaneous Met-driven tumors with high penetrance and short latency... - Antiangiogenic and anti-invasive effects of sunitinib on experimental human glioblastomaSophie De Bouard
GRECAN, Centre Francois Baclesse, Universié de Caen Basse Normandie, 14076 Caen, France
Neuro Oncol 9:412-23. 2007..Sunitinib exhibited potent antiangiogenic activity that was associated with a meaningful prolongation of survival of mice bearing intracerebral GBM. These data support the potential utility of sunitinib in the treatment of GBM... - Preclinical efficacy of the c-Met inhibitor CE-355621 in a U87 MG mouse xenograft model evaluated by 18F-FDG small-animal PETJeffrey R Tseng
Molecular Imaging Program at Stanford, Bio X Program, and Department of Radiology, Stanford University, Stanford, California 94305 5427, USA
J Nucl Med 49:129-34. 2008..The purpose of this study was to evaluate the efficacy of CE-355621, a novel antibody against c-Met, in a subcutaneous U87 MG xenograft mouse model using (18)F-FDG small-animal PET... - A selective small molecule c-MET Inhibitor, PHA665752, cooperates with rapamycinPatrick C Ma
Section of Hematology/Oncology, Department of Medicine, Pritzker School of Medicine, University of Chicago Medical Center, 5841 South Maryland Avenue, Chicago, IL 60637, USA
Clin Cancer Res 11:2312-9. 2005..PHA665752 is also active against H441 NSCLC cells. The c-MET inhibitor can cooperate with rapamycin in therapeutic inhibition of NSCLC, and in vivo studies of this combination against c-MET expressing cancers would be merited...