Phase I study of sorafenib in patients with refractory or relapsed acute leukemias
暂无分享,去创建一个
M. Konopleva | M. Andreeff | H. Kantarjian | J. Cortes | S. Verstovsek | F. Ravandi | G. Borthakur | Weiguo Zhang | J. Wright | S. Faderl | Sheela Mathews
[1] B. Leber,et al. A randomized phase I clinical and biologic study of two schedules of sorafenib in patients with myelodysplastic syndrome or acute myeloid leukemia: a NCIC (National Cancer Institute of Canada) Clinical Trials Group Study , 2010, Leukemia & lymphoma.
[2] M. Konopleva,et al. Selective FLT3 inhibitor FI-700 neutralizes Mcl-1 and enhances p53-mediated apoptosis in AML cells with activating mutations of FLT3 through Mcl-1/Noxa axis , 2010, Leukemia.
[3] M. Andreeff,et al. Phase I/II study of idarubicin (Ida), high-dose ara-C, and sorafenib (S) in patients (pts) younger than 65 years with acute myeloid leukemia (AML). , 2016, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[4] H. Kantarjian,et al. AC220, a Potent, Selective, Second Generation FLT3 Receptor Tyrosine Kinase (RTK) Inhibitor, in a First-in-Human (FIH) Phase 1 AML Study. , 2009 .
[5] M. Eilers,et al. Compassionate use of sorafenib in FLT3-ITD-positive acute myeloid leukemia: sustained regression before and after allogeneic stem cell transplantation. , 2009, Blood.
[6] E. Estey,et al. Targeting the leukemia microenvironment by CXCR4 inhibition overcomes resistance to kinase inhibitors and chemotherapy in AML. , 2009, Blood.
[7] B. Smith,et al. Phase I dose escalation trial of sorafenib as a single agent for adults with relapsed and refractory acute leukemias. , 2009, Journal of Clinical Oncology.
[8] J. Cerhan,et al. Genetic variation in caspase genes and risk of non-Hodgkin lymphoma: a pooled analysis of 3 population-based case-control studies. , 2009, Blood.
[9] S. Akinaga,et al. A pharmacodynamic study of the FLT3 inhibitor KW-2449 yields insight into the basis for clinical response. , 2009, Blood.
[10] R. Engh,et al. FMS-like tyrosine kinase 3-internal tandem duplication tyrosine kinase inhibitors display a nonoverlapping profile of resistance mutations in vitro. , 2009, Cancer research.
[11] I. Bernstein,et al. Role for genetic anticipation in Lynch syndrome. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[12] M. Konopleva,et al. Mutant FLT3: a direct target of sorafenib in acute myelogenous leukemia. , 2008, Journal of the National Cancer Institute.
[13] M. Caligiuri,et al. FLT3 D835/I836 mutations are associated with poor disease-free survival and a distinct gene-expression signature among younger adults with de novo cytogenetically normal acute myeloid leukemia lacking FLT3 internal tandem duplications. , 2008, Blood.
[14] M. Konopleva,et al. Sorafenib induces apoptosis of AML cells via Bim-mediated activation of the intrinsic apoptotic pathway , 2008, Leukemia.
[15] W. Hiddemann,et al. BH3 mimetic ABT-737 neutralizes resistance to FLT3 inhibitor treatment mediated by FLT3-independent expression of BCL2 in primary AML blasts , 2007, Leukemia.
[16] D. Auclair,et al. Antitumor activity of sorafenib in FLT3-driven leukemic cells , 2007, Leukemia.
[17] H. Kantarjian,et al. Phase IB Study of PKC412, an Oral FLT3 Kinase Inhibitor, in Sequential and Simultaneous Combinations with Daunorubicin and Cytarabine (DA) Induction and High-Dose Cytarabine Consolidation in Newly Diagnosed Adult Patients (pts) with Acute Myeloid Leukemia (AML) under Age 61. , 2006 .
[18] Steven M Kornblau,et al. Simultaneous activation of multiple signal transduction pathways confers poor prognosis in acute myelogenous leukemia. , 2004, Blood.
[19] S. Wilhelm,et al. Sorafenib (BAY 43-9006, Nexavar), a dual-action inhibitor that targets RAF/MEK/ERK pathway in tumor cells and tyrosine kinases VEGFR/PDGFR in tumor vasculature. , 2006, Methods in enzymology.
[20] R. Stone,et al. Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain. , 2006, Blood.
[21] G. Gores,et al. The role of Mcl-1 downregulation in the proapoptotic activity of the multikinase inhibitor BAY 43-9006 , 2005, Oncogene.
[22] Jeffrey W. Clark,et al. Safety and Pharmacokinetics of the Dual Action Raf Kinase and Vascular Endothelial Growth Factor Receptor Inhibitor, BAY 43-9006, in Patients with Advanced, Refractory Solid Tumors , 2005, Clinical Cancer Research.
[23] D. Hedley,et al. Raf kinase as a target for anticancer therapeutics , 2005, Molecular Cancer Therapeutics.
[24] Dirk Strumberg,et al. Phase I clinical and pharmacokinetic study of the Novel Raf kinase and vascular endothelial growth factor receptor inhibitor BAY 43-9006 in patients with advanced refractory solid tumors. , 2005, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[25] M. Konopleva,et al. Quantitative single cell determination of ERK phosphorylation and regulation in relapsed and refractory primary acute myeloid leukemia , 2005, Leukemia.
[26] E. Estey,et al. Patients with acute myeloid leukemia and an activating mutation in FLT3 respond to a small-molecule FLT3 tyrosine kinase inhibitor, PKC412 , 2004 .
[27] H. Kantarjian,et al. Phase IB Study of PKC412, an Oral FLT3 Kinase Inhibitor, in Sequential and Simultaneous Combinations with Daunorubicin and Cytarabine (DA) Induction and High-Dose Cytarabine Consolidation in Newly Diagnosed Patients with AML. , 2004 .
[28] M. Sporn,et al. The Synthetic Triterpenoid 2-Cyano-3,12-dioxooleana-1,9-dien-28-oic Acid Induces Caspase-Dependent and -Independent Apoptosis in Acute Myelogenous Leukemia , 2004, Cancer Research.
[29] B. Smith,et al. In vitro studies of a FLT3 inhibitor combined with chemotherapy: sequence of administration is important to achieve synergistic cytotoxic effects. , 2004, Blood.
[30] B. Löwenberg,et al. Relation between CXCR-4 expression, Flt3 mutations, and unfavorable prognosis of adult acute myeloid leukemia. , 2004, Blood.
[31] H. Kantarjian,et al. Single-agent CEP-701, a novel FLT3 inhibitor, shows biologic and clinical activity in patients with relapsed or refractory acute myeloid leukemia. , 2004, Blood.
[32] C. Bloomfield,et al. Revised recommendations of the International Working Group for Diagnosis, Standardization of Response Criteria, Treatment Outcomes, and Reporting Standards for Therapeutic Trials in Acute Myeloid Leukemia. , 2003, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[33] Steven M Kornblau,et al. The mitogen-activated protein kinase signaling module as a therapeutic target in hematologic malignancies. , 2003, Reviews in clinical and experimental hematology.
[34] J. Griffin,et al. The roles of FLT3 in hematopoiesis and leukemia. , 2002, Blood.
[35] E. Estey,et al. Therapeutic targeting of the MEK/MAPK signal transduction module in acute myeloid leukemia. , 2001, The Journal of clinical investigation.
[36] S. Kornblau,et al. Regulation of Bcl2 phosphorylation and potential significance for leukemic cell chemoresistance. , 2000, Journal of the National Cancer Institute. Monographs.
[37] S. Zhao,et al. Cell-surface exposure of phosphatidylserine correlates with the stage of fludarabine-induced apoptosis in chronic lymphocytic leukemia and expression of apoptosis-regulating genes. , 2000, Cytometry.
[38] T. Naoe,et al. Tandem-duplicated Flt3 constitutively activates STAT5 and MAP kinase and introduces autonomous cell growth in IL-3-dependent cell lines , 2000, Oncogene.
[39] H. Kaneko,et al. Internal tandem duplication of the flt3 gene found in acute myeloid leukemia. , 1996, Leukemia.