BibSonomyburst/user/kanefendt/SU11248BibSonomy RSS feed for /user/kanefendt/SU112482012-02-16T18:56:47+01:00http://www.bibsonomy.org/bibtex/2f8621c86345a8b8fe2693fc3e8855cee/kanefendtkanefendt2010-02-05T11:28:39+01:00Cells Endothelial Monocytes Population SU11248 Tyrosine cells identify <span class="authorEditorList"><a href="/author/Norden-Zfoni">Anat Norden-Zfoni</a>, <a href="/author/Desai">Jayesh Desai</a>, <a href="/author/Manola">Judith Manola</a>, <a href="/author/Beaudry">Paul Beaudry</a>, <a href="/author/Force">Jeremy Force</a>, <a href="/author/Maki">Robert Maki</a>, <a href="/author/Folkman">Judah Folkman</a>, <a href="/author/Bello">Carlo Bello</a>, <a href="/author/Baum">Charles Baum</a>, <a href="/author/DePrimo">Sam E. DePrimo</a>, <a href="/author/Shalinsky">David R. Shalinsky</a>, <a href="/author/Demetri">Goerge D. Demetri</a>, and <a href="/author/Heymach">John V. Heymach</a> </span><em>Clin Cancer Res</em> <em>13(9):2643-2650</em> (<em>2007</em>)Fri Feb 05 11:28:39 CET 2010Clin Cancer Res92643-2650Blood-Based Biomarkers of SU11248 Activity and Clinical Outcome in Patients with Metastatic Imatinib-Resistant Gastrointestinal Stromal Tumor132007Cells Endothelial Monocytes Population SU11248 Tyrosine cells identify Purpose: There is an unmet need for noninvasive markers to measure the biological effects of targeted agents, particularly those inhibiting the vascular endothelial growth factor (VEGF) receptor (VEGFR) pathway, and identify patients most likely to benefit from treatment. In this study, we investigated potential blood-based biomarkers for SU11248 (sunitinib malate), a multitargeted tyrosine kinase inhibitor, in patients with metastatic imatinib-refractory gastrointestinal stromal tumors. Experimental Design: Patients (n = 73) enrolled in a phase I/II trial received SU11248 daily for 14 or 28 days followed by 14 days without treatment per cycle. Clinical benefit was defined as progression-free survival of >6 months. We assessed plasma markers, including VEGF and soluble VEGFR-2 (sVEGFR-2), and two cellular populations bearing VEGF receptors: monocytes and, in a subset of patients, mature circulating endothelial cells (CEC). Results: Compared to patients with progressive disease, patienthttp://www.bibsonomy.org/bibtex/2c051401322a1f486c5abd101be04bb7c/kanefendtkanefendt2010-02-05T11:28:39+01:00Outcome Proteins Research SU11248 Treatment Tyrosine analysis methods protein response therapy <span class="authorEditorList"><a href="/author/Deprimo">S. E. Deprimo</a>, <a href="/author/Friece">C. Friece</a>, <a href="/author/Huang">X. Huang</a>, <a href="/author/Smeraglia">J. Smeraglia</a>, <a href="/author/Sherman">L. Sherman</a>, <a href="/author/Collier">M. Collier</a>, <a href="/author/Baum">C. Baum</a>, <a href="/author/Elias">A. D. Elias</a>, <a href="/author/Burstein">H. J. Burstein</a>, and <a href="/author/Miller">K. D. Miller</a> </span><em>J Clin Oncol Meeting Abstracts</em> <em>24(18_suppl):578</em> (<em>2006</em>)Fri Feb 05 11:28:39 CET 2010J Clin Oncol (Meeting Abstracts)18_suppl578Effect of treatment with sunitinib malate, a multitargeted tyrosine kinase inhibitor, on circulating plasma levels of VEGF, soluble VEGF receptors 2 and 3, and soluble KIT in patients with metastatic breast cancer242006Outcome Proteins Research SU11248 Treatment Tyrosine analysis methods protein response therapy 578 Background: Sunitinib malate (SU11248) is a multitargeted tyrosine kinase inhibitor with antitumor and antiangiogenic activity that specifically inhibits VEGFR, PDGFR, KIT, RET and FLT3. In a phase II trial of 64 patients with refractory, metastatic breast cancer, sunitinib treatment resulted in an [~]11% objective response rate (Miller et al, ASCO 2005). To characterize potential biomarkers of biological response to sunitinib, we analyzed plasma levels of a panel of soluble proteins from patients in this trial. Methods: Patients received sunitinib in 6-week cycles comprised of 50 mg/day for 4 weeks followed by 2 weeks off treatment. Pre-dose plasma samples from 62 patients were obtained on days 1, 14, and 28 of the first cycle and days 1 and 28 of subsequent cycles. Plasma levels of VEGF, soluble VEGF receptor 2 (sVEGFR-2), soluble KIT (sKIT), and a novel biomarker, sVEGFR-3, were measured via ELISA analysis. Results: Plasma levels of each protein were modulated in most patients dhttp://www.bibsonomy.org/bibtex/2f38143fbe04ea33b5ecd4279ec2ce263/kanefendtkanefendt2010-02-05T11:28:39+01:00Research SU11248 <span class="authorEditorList"><a href="/author/DePrimo">Samuel E. DePrimo</a>, <a href="/author/Toner">Guy Toner</a>, <a href="/author/Mitchell">Paul Mitchell</a>, <a href="/author/Boer">Richard Boer</a>, <a href="/author/Gibbs">Peter Gibbs</a>, <a href="/author/Hicks">Rodney Hicks</a>, <a href="/author/McArthur">Grant McArthur</a>, <a href="/author/Brega">Nicoletta Brega</a>, <a href="/author/McCarthy">Timothy McCarthy</a>, and <a href="/author/Bello">Carlo Bello</a> (Eds.). </span><em> 47, </em><em>Philadelphia, PA, </em><em>AACR, </em>(<em>2006</em>)Fri Feb 05 11:28:39 CET 2010Philadelphia, PAModulation of biomarkers of angiogenesis during treatment with SU11248 (sunitinib malate) in patients with advanced malignancies: Proceedings of the 97th Annual Meeting of the American Association for Cancer Research472006Research SU11248 http://www.bibsonomy.org/bibtex/24927b533c5bbdadbcdd4591c087cdbf4/kanefendtkanefendt2010-02-05T11:28:39+01:00&amp; 3 Acute Aged Clearance Endothelial Factor Female Follow-Up Genotype Growth Human Humans Hypertension Indoles Kinase Kinases Leukemia Lung Male Metabolic Middle Mutation Myeloid Pharmacokinetics Platelet-Derived Protein-Tyrosine Proteins Proto-Oncogene Pyrroles Rate Receptor Receptors Research SU11248 Studies Tyrosine Vascular analysis antagonists cells drug fms-Like genetics inhibitors protein response therapeutic therapy toxicity use <span class="authorEditorList"><a href="/author/Fiedler">W. Fiedler</a>, <a href="/author/Serve">H. Serve</a>, <a href="/author/Dohner">H. Dohner</a>, <a href="/author/Schwittay">M. Schwittay</a>, <a href="/author/Ottmann">O. G. Ottmann</a>, <a href="/author/O&#039;Farrell">A. M. O&#039;Farrell</a>, <a href="/author/Bello">C. L. Bello</a>, <a href="/author/Allred">R. Allred</a>, <a href="/author/Manning">W. C. Manning</a>, <a href="/author/Cherrington">J. M. Cherrington</a>, <a href="/author/Louie">S. G. Louie</a>, <a href="/author/Hong">W. Hong</a>, <a href="/author/Brega">N. M. Brega</a>, <a href="/author/Massimini">G. Massimini</a>, <a href="/author/Scigalla">P. Scigalla</a>, <a href="/author/Berdel">W. E. Berdel</a>, and <a href="/author/Hossfeld">D. K. Hossfeld</a> </span><em>Blood</em> <em>105(3):986-993</em> (<em>2005</em>)Fri Feb 05 11:28:39 CET 2010Blood3986-993A phase 1 study of SU11248 in the treatment of patients with refractory or resistant acute myeloid leukemia (AML) or not amenable to conventional therapy for the disease1052005& 3 Acute Aged Clearance Endothelial Factor Female Follow-Up Genotype Growth Human Humans Hypertension Indoles Kinase Kinases Leukemia Lung Male Metabolic Middle Mutation Myeloid Pharmacokinetics Platelet-Derived Protein-Tyrosine Proteins Proto-Oncogene Pyrroles Rate Receptor Receptors Research SU11248 Studies Tyrosine Vascular analysis antagonists cells drug fms-Like genetics inhibitors protein response therapeutic therapy toxicity use Fifteen patients with refractory AML were treated in a phase 1 study with SU11248, an oral kinase inhibitor of fms-like tyrosine kinase 3 (Flt3), Kit, vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF) receptors. Separate cohorts of patients received SU11248 for 4-week cycles followed by either a 2- or a 1-week rest period. At the starting dose level of 50 mg (n = 13), no dose-limiting toxicities were observed. The most frequent grade 2 toxicities were edema, fatigue, and oral ulcerations. Two fatal bleedings possibly related to the disease, one from a concomitant lung cancer and one cerebral bleeding, were observed. At the 75 mg dose level (n = 2), one case each of grade 4 fatigue, hypertension, and cardiac failure was observed, and this dose level was abandoned. All patients with FLT3 mutations (n = 4) had morphologic or partial responses compared with 2 of 10 evaluable patients with wild-type FLT3. Responses, although longer in patients with mutated