Affiliation: Novartis Institutes for BioMedical Research
- Imatinib mesylate attenuates fibrosis in coxsackievirus b3-induced chronic myocarditisCarola Leipner
Institute of Virology, Medical Faculty, Friedrich Schiller University, Jena, Germany
Cardiovasc Res 79:118-26. 2008..To test if PDGF stimulation of resident fibroblasts causally contributes to fibrosis, we employed inhibition of PDGF receptor signalling with the orally available kinase inhibitor Imatinib...
- [Bcr-Abl inhibition as molecular therapy approach in chronic myeloid leukemia]Elisabeth Buchdunger
Präklinische Forschung Onkologie, Novartis Pharma AG, Basel, Schweiz
Med Klin (Munich) 97:2-6. 2002..Recent studies with clinical samples from resistant patients have shown that point mutations in the kinase domain of Bcr-Abl play a role in the development of resistance to STI571...
- Pharmacology of imatinib (STI571)Elisabeth Buchdunger
Oncology Research Department, Novartis Pharma AG, CH 4002 Basel, Switzerland
Eur J Cancer 38:S28-36. 2002..The pharmacology of imatinib and its activity in various tumor models is discussed...
- Glivec (STI571, imatinib), a rationally developed, targeted anticancer drugRenaud Capdeville
Novartis Pharma AG, S 27 2 033, CH 4002 Basel, Switzerland
Nat Rev Drug Discov 1:493-502. 2002..Here, we describe how this programme led to the discovery and continuing development of Glivec (Gleevec in the United States), the first selective tyrosine-kinase inhibitor to be approved for the treatment of a cancer...
- Protein kinases as targets for anticancer agents: from inhibitors to useful drugsDoriano Fabbro
Department of Oncology, Novartis Pharma Inc, WKL 125 4 10, CH 4002, Basel, Switzerland
Pharmacol Ther 93:79-98. 2002..Phase I/II studies demonstrated that STI571 is well tolerated, and that it showed promising hematological and cytogenetic responses in CML and clinical responses in the c-Kit-driven gastrointestinal tumors...
- Imatinib mesylate is a potent inhibitor of the ABCG2 (BCRP) transporter and reverses resistance to topotecan and SN-38 in vitroPeter J Houghton
Department of Molecular Pharmacology, St Jude Children s Research Hospital, Memphis, Tennessee 38105 2794, USA
Cancer Res 64:2333-7. 2004..These results suggest that imatinib mesylate inhibits the function of ABCG2 but is not a substrate for this transporter...
- Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemiaYiguo Hu
The Jackson Laboratory, 600 Main St, Bar Harbor, Maine 04609, USA
Nat Genet 36:453-61. 2004..These results implicate Src family kinases as therapeutic targets in Ph(+) B-ALL and suggest that simultaneous inhibition of Src and Bcr-Abl kinases may benefit individuals with Ph(+) acute leukemia...
- The insulin-like growth factor-I (IGF-I) receptor kinase inhibitor NVP-ADW742, in combination with STI571, delineates a spectrum of dependence of small cell lung cancer on IGF-I and stem cell factor signalingG Sakuntala Warshamana-Greene
Department of Medicine, Virginia Commonwealth University and McGuire Veterans Affairs Medical Center, Richmond, Virginia 23249, USA
Mol Cancer Ther 3:527-35. 2004..These observations suggest that, in tumors in which critical signal transduction pathways can be activated by alternative receptors, optimal therapy may require inhibition of multiple receptors...
- The development of imatinib as a therapeutic agent for chronic myeloid leukemiaMichael Deininger
Oregon Health and Science University Cancer Institute, 3181 SW Sam Jackson Park Rd, Mailcode L592, Portland, OR 97239, USA
Blood 105:2640-53. 2005..In this manuscript, we review the preclinical and clinical development of imatinib for the therapy of CML, resistance and strategies that may help to eliminate resistant or residual leukemia...
- The insulin-like growth factor-I receptor kinase inhibitor, NVP-ADW742, sensitizes small cell lung cancer cell lines to the effects of chemotherapyG Sakuntala Warshamana-Greene
Department of Medicine, Virginia Commonwealth University and McGuire Veterans Affairs Medical Center, Richmond, VA 23249, USA
Clin Cancer Res 11:1563-71. 2005..The purpose of this study was to determine whether the novel IGF-I receptor (IGF-IR) kinase inhibitor, NVP-ADW742, sensitizes SCLC cell lines to etoposide and carboplatin, which are commonly used in the treatment of SCLC...
- Oral imatinib mesylate (STI571/gleevec) improves the efficacy of local intravascular vascular endothelial growth factor-C gene transfer in reducing neointimal growth in hypercholesterolemic rabbitsOlli Leppanen
Ludwig Institute for Cancer Research, Uppsala, Sweden
Circulation 109:1140-6. 2004....
- STI571 enhances the therapeutic index of epothilone B by a tumor-selective increase of drug uptakeKristian Pietras
Ludwig Institute for Cancer Research, SE 751 24 Uppsala, Sweden
Clin Cancer Res 9:3779-87. 2003....
- Platelet-derived growth factor receptor inhibition reduces allograft arteriosclerosis of heart and aorta in cholesterol-fed rabbitsRoope K Sihvola
Cardiopulmonary Research Group, Transplantation Laboratory, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland
Transplantation 75:334-9. 2003..In this study, we tested the effect of STI 571, a novel orally active protein tyrosine kinase (PTK) inhibitor selective for PDGF receptor (PDGF-R) on transplant and accelerated arteriosclerosis in hypercholesterolemic rabbits...
- Imatinib mesylate (STI-571) reduces Bcr-Abl-mediated vascular endothelial growth factor secretion in chronic myelogenous leukemiaJohn M L Ebos
Molecular and Cell Biology Research, Sunnybrook and Women s College Health Sciences Centre, Toronto, Ontario, Canada M4N 3M5
Mol Cancer Res 1:89-95. 2002..Taken together, our results implicate BCR-ABL as a possible regulator of CML angiogenesis and raise the possibility that STI-571 could mediate some of its anti-CML properties in vivo through an angiogenesis-dependent mechanism...
- Dual-specific Src and Abl kinase inhibitors, PP1 and CGP76030, inhibit growth and survival of cells expressing imatinib mesylate-resistant Bcr-Abl kinasesMarkus Warmuth
Klinische Kooperationsgruppe für Gentherapie, GSF Forschungszentrum für Umwelt und Gesundheit, Munich, Germany
Blood 101:664-72. 2003..The results suggest that the use of Src kinase inhibitors is a potential strategy to prevent or overcome clonal evolution of imatinib mesylate resistance in Bcr-Abl(+) leukemia...
- Inhibition of PDGF receptor signaling in tumor stroma enhances antitumor effect of chemotherapyKristian Pietras
Ludwig Institute for Cancer Research, SE 751 24 Uppsala, Sweden
Cancer Res 62:5476-84. 2002..In conclusion, our study identifies inhibition of PDGF signaling in tumor stroma as a novel, possibly general strategy for enhancement of the therapeutic effects chemotherapy...
- Analysis of the structural basis of specificity of inhibition of the Abl kinase by STI571Amie S Corbin
Division of Hematology and Medical Oncology, Oregon Health and Science University, Portland, Oregon 97201, USA
J Biol Chem 277:32214-9. 2002....