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

References

• Tallman MS, Gilliland DG, Rowe JM. Drug therapy for acute myeloid leukemia. Blood 2005;106:1154–1163.
   PubMed Web of Science ®Google Scholar
• Cassileth PA, Harrington DP, Appelbaum FR, et al Chemotherapy compared with autologous or allogeneic bone marrow transplantation in the management of acute myeloid leukemia in first remission. N Engl J Med 1998;339:1649–1656.
   PubMed Web of Science ®Google Scholar
• Breems DA, Boogaerts MA, Dekker AW, et al Autologous bone marrow transplantation as consolidation therapy in the treatment of adult patients under 60 years with acute myeloid leukaemia in first complete remission: a prospective randomized Dutch-Belgian Haemato-Oncology Co-operative Group (HOVON) and Swiss Group for Clinical Cancer Research (SAKK) trial. Br J Haematol 2005;128:59–65.
   PubMed Web of Science ®Google Scholar
• van der Holt B, Lowenberg B, Burnett AK, et al The value of the MDR1 reversal agent PSC-833 in addition to daunorubicin and cytarabine in the treatment of elderly patients with previously untreated acute myeloid leukemia (AML), in relation to MDR1 status at diagnosis. Blood 2005;106:2646–2654.
   PubMed Web of Science ®Google Scholar
• Amadori S, Suciu S, Jehn U, et al Use of glycosylated recombinant human G-CSF (lenograstim) during and/or after induction chemotherapy in patients 61 years of age and older with acute myeloid leukemia: final results of AML-13, a randomized phase-3 study. Blood 2005;106:27–34.
   PubMed Web of Science ®Google Scholar
• Silverman LR, Demakos EP, Peterson BL, et al Randomized controlled trial of azacitidine in patients with the myelodysplastic syndrome: a study of the Cancer and Leukemia Group B. J Clin Oncol 2002;20:2429–2440.
   PubMed Web of Science ®Google Scholar
• Gilliland DG, Griffin JD. The roles of FLT3 in hematopoiesis and leukemia. Blood 2002;100:1532–1542.
   PubMed Web of Science ®Google Scholar
• Spiekermann K, Bagrintseva K, Schwab R, Schmieja K, Hiddemann W. Over-expression and constitutive activation of FLT3 induces STAT5 activation in primary acute myeloid leukemia blast cells. Clin Cancer Res 2003;9:2140–2150.
   PubMed Web of Science ®Google Scholar
• Care RS, Valk PJ, Goodeve AC, et al Incidence and prognosis of c-KIT and FLT3 mutations in core binding factor (CBF) acute myeloid leukaemias. Br J Haematol 2003;121:775–777.
   PubMed Web of Science ®Google Scholar
• Illmer T, Thiede C, Fredersdorf A, et al Activation of the RAS pathway is predictive for a chemosensitive phenotype of acute myelogenous leukemia blasts. Clin Cancer Res 2005;11:3217–3224.
   PubMed Web of Science ®Google Scholar
• Chong H, Vikis HG, Guan KL. Mechanisms of regulating the Raf kinase family. Cell Signal 2003;15:463–469.
   PubMed Web of Science ®Google Scholar
• Beeram M, Patnaik A, Rowinsky EK. Raf: a strategic target for therapeutic development against cancer. J Clin Oncol 2005;23:6771–6790.
   PubMed Web of Science ®Google Scholar
• Frohling S, Scholl C, Gilliland DG, Levine RL. Genetics of myeloid malignancies: pathogenetic and clinical implications. J Clin Oncol 2005;23:6285–6295.
   PubMed Web of Science ®Google Scholar
• Staber PB, Linkesch W, Zauner D, et al Common alterations in gene expression and increased proliferation in recurrent acute myeloid leukemia. Oncogene 2004;23:894–904.
   PubMed Web of Science ®Google Scholar
• Karp JE, Lancet JE, Kaufmann SH, et al Clinical and biologic activity of the farnesyltransferase inhibitor R115777 in adults with refractory and relapsed acute leukemias: a phase 1 clinical-laboratory correlative trial. Blood 2001;97:3361–3369.
   PubMed Web of Science ®Google Scholar
• Zimmerman TM, Harlin H, Odenike OM, et al Dose-ranging pharmacodynamic study of tipifarnib (R115777) in patients with relapsed and refractory hematologic malignancies. J Clin Oncol 2004;22:4816–4822.
   PubMed Web of Science ®Google Scholar
• Gianpaolo-Ostravage C, Carter C, Hibner B. Anti-tumor efficacy of the orally active raf kinase inhibitor sorafenib in human tumor xenograft models. Proc Am Assoc Cancer Res 2001;42:923.
   Google Scholar
• Wilhelm S, Chien DS. Sorafenib: preclinical data. Curr Pharm Des 2002;8:2255–2257.
   PubMed Web of Science ®Google Scholar
• Wilhelm SM, Carter C, Tang L, et al Sorafenib exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis. Cancer Res 2004;64:7099–7109.
   PubMed Web of Science ®Google Scholar
• Meng XW, Lee SH, Dai H, et al Mcl-1 as a buffer for proapoptotic Bcl-2 family members during TRAIL-induced apoptosis: a mechanistic basis for sorafenib (Bay 43-9006)-induced TRAIL sensitization. J Biol Chem 2007;282:29831–29846.
   PubMed Web of Science ®Google Scholar
• Rahmani M, Davis EM, Bauer C, Dent P, Grant S. Apoptosis induced by the kinase inhibitor BAY 43-9006 in human leukemia cells involves down-regulation of Mcl-1 through inhibition of translation. J Biol Chem 2005;280:35217–35227.
   PubMed Web of Science ®Google Scholar
• Cheson BD, Cassileth PA, Head DR, et al Report of the National Cancer Institute-sponsored workshop on definitions of diagnosis and response in acute myeloid leukemia. J Clin Oncol 1990;8:813–819.
   PubMed Web of Science ®Google Scholar
• Cheson BD, Bennett JM, Kantarjian H, et al Report of an international working group to standardize response criteria for myelodysplastic syndromes. Blood 2000;96:3671–3674.
   PubMed Web of Science ®Google Scholar
• Chow S, Patel H, Hedley DW. Measurement of MAP kinase activation by flow cytometry using phospho-specific antibodies to MEK and ERK: potential for pharmacodynamic monitoring of signal transduction inhibitors. Cytometry 2001;46:72–78.
   PubMedGoogle Scholar
• Byrd JC, Mrozek K, Dodge RK, et al Pretreatment cytogenetic abnormalities are predictive of induction success, cumulative incidence of relapse, and overall survival in adult patients with de novo acute myeloid leukemia: results from Cancer and Leukemia Group B (CALGB 8461). Blood 2002;100:4325–4336.
   PubMed Web of Science ®Google Scholar
• Auclair D, Miller D, Yatsula V, et al Antitumor activity of sorafenib in FLT3-driven leukemic cells. Leukemia 2007;21:439–445.
   PubMed Web of Science ®Google Scholar
• Awada A, Hendlisz A, Gil T, et al Phase I safety and pharmacokinetics of sorafenib administered for 21 days on/7 days off in patients with advanced, refractory solid tumours. Br J Cancer 2005;92:1855–1861.
   PubMed Web of Science ®Google Scholar
• Strumberg D, Richly H, Hilger RA, et al Phase I clinical and pharmacokinetic study of the novel Raf kinase and vascular endothelial growth factor receptor inhibitor sorafenib in patients with advanced refractory solid tumors. J Clin Oncol 2005;23:965–972.
   PubMed Web of Science ®Google Scholar
• Zhang W, Konopleva M, Shi YX, et al Mutant FLT3: a direct target of sorafenib in acute myelogenous leukemia. J Natl Cancer Inst 2008;100:184–198.
   PubMed Web of Science ®Google Scholar
• Padro T, Bieker R, Ruiz S, et al Overexpression of vascular endothelial growth factor (VEGF) and its cellular receptor KDR (VEGFR-2) in the bone marrow of patients with acute myeloid leukemia. Leukemia 2002;16:1302–1310.
   PubMed Web of Science ®Google Scholar
• Santos SC, Dias S. Internal and external autocrine VEGF/KDR loops regulate survival of subsets of acute leukemia through distinct signaling pathways. Blood 2004;103:3883–3889.
   PubMed Web of Science ®Google Scholar
• Burnett AK, Milligan D, Prentice AG, et al A comparison of low-dose cytarabine and hydroxyurea with or without all-trans retinoic acid for acute myeloid leukemia and high-risk myelodysplastic syndrome in patients not considered fit for intensive treatment. Cancer 2007;109:1114–1124.
   PubMed Web of Science ®Google Scholar