A phase-1 study of dasatinib plus all-trans retinoic acid in acute myeloid leukemia

References

• Johnson DE. Src family kinases and the MEK/ERK pathway in the regulation of myeloid differentiation and myeloid leukemogenesis. Adv Enzyme Regul. 2008;48:98–112.
   PubMedGoogle Scholar
• Willman CL, Stewart CC, Griffith JK, et al. Differential expression and regulation of the c-src and c-fgr protooncogenes in myelomonocytic cells. Proc Natl Acad Sci USA. 1987;84:4480–4484.
   PubMed Web of Science ®Google Scholar
• Willman CL, Stewart CC, Longacre TL, et al. Expression of the c-fgr and hck protein-tyrosine kinases in acute myeloid leukemic blasts is associated with early commitment and differentiation events in the monocytic and granulocytic lineages. Blood. 1991;77:726–734.
   PubMed Web of Science ®Google Scholar
• Thomas SM, Brugge JS. Cellular functions regulated by Src family kinases. Annu Rev Cell Dev Biol. 1997;13:513–609.
   PubMed Web of Science ®Google Scholar
• Corey SJ, Anderson SM. Src-related protein tyrosine kinases in hematopoiesis. Blood. 1999;93:1–14.
   PubMed Web of Science ®Google Scholar
• Abram CL, Courtneidge SA. Src family tyrosine kinases and growth factor signaling. Exp Cell Res. 2000;254:1–13.
   PubMed Web of Science ®Google Scholar
• Mermel CH, McLemore ML, Liu F, et al. Src family kinases are important negative regulators of G-CSF-dependent granulopoiesis. Blood. 2006;108:2562–2568.
   PubMed Web of Science ®Google Scholar
• Harder KW, Parsons LM, Armes J, et al. Gain- and loss-of-function Lyn mutant mice define a critical inhibitory role for Lyn in the myeloid lineage. Immunity. 2001;5:603–615.
   Google Scholar
• Lowell CA, Fumagalli L, Berton G. Deficiency of Src family kinases p59/61hck and p58c-fgr results in defective adhesion-dependent neutrophil functions. J Cell Biol. 1996;33:895–910.
   Google Scholar
• Miranda MB, Redner RL, Johnson DE. Inhibition of Src family kinases enhances retinoic acid induced gene expression and myeloid differentiation. Mol Cancer Ther. 2007;6:3081–3090.
   PubMed Web of Science ®Google Scholar
• Congleton J, MacDonald R, Yen A. Src inhibitors, PP2 and dasatinib, increase retinoic acid-induced association of Lyn and c-Raf (S259) and enhance MAPK-dependent differentiation of myeloid leukemia cells. Leukemia. 2012;26:1180–1188.
   PubMed Web of Science ®Google Scholar
• Melnick A, Licht JD. Deconstructing a disease: RARalpha, its fusion partners, and their roles in the pathogenesis of acute promyelocytic leukemia. Blood. 1999;93:3167–3215.
   PubMed Web of Science ®Google Scholar
• Kropf PL, Wang L, Zang Y, et al. Dasatinib promotes ATRA-induced differentiation of AML cells. Leukemia. 2010;24:663–665.
   PubMed Web of Science ®Google Scholar
• Miranda MB, Johnson DE. Signal transduction pathways that contribute to myeloid differentiation. Leukemia. 2007;21:1363–1377.
   PubMed Web of Science ®Google Scholar
• Schittenhelm MM, Shiraga S, Schroeder A, et al. Dasatinib (BMS-354825), a dual SRC/ABL kinase inhibitor, inhibits the kinase activity of wild-type, juxtamembrane, and activation loop mutant KIT isoforms associated with human malignancies. Cancer Res. 2006;66:473–481.
   PubMed Web of Science ®Google Scholar
• Collins SJ. The role of retinoids and retinoic acid receptors in normal hematopoiesis. Leukemia. 2002;16:1896–1905.
   PubMed Web of Science ®Google Scholar
• Campo E, Swerdlow SH, Harris NL, et al. The 2008 WHO classification of lymphoid neoplasms and beyond: evolving concepts and practical applications. Blood. 2011;117:5019–5032.
   PubMed Web of Science ®Google Scholar
• Greenberg P, Cox C, LeBeau MM, et al. International scoring system for evaluating prognosis in myelodysplastic syndromes. Blood. 1997;89:2079–2088.
   PubMed Web of Science ®Google Scholar
• Twardowski PW, Beumer JH, Chen CS, et al. A phase II trial of dasatinib in patients with metastatic castration-resistant prostate cancer treated previously with chemotherapy. Anticancer Drugs. 2013;24:743–753.
   PubMed Web of Science ®Google Scholar
• Conley BA, Egorin MJ, Sridhara R, et al. Phase I clinical trial of all-trans-retinoic acid with correlation of its pharmacokinetics and pharmacodynamics. Cancer Chemother Pharmacol. 1997;39:291–299.
   PubMed Web of Science ®Google Scholar
• Lehmann S, Bengtzen S, Broberg U, et al. Effects of retinoids on cell toxicity and apoptosis in leukemic blast cells from patients with non-M3 AML. Leuk Res. 2000;24:19–25.
   PubMed Web of Science ®Google Scholar
• Qian SX, Li JY, Hong M, et al. Acute myeloid leukemia in four patients with t(8;21) treated with all-trans retinoic acid as a single agent. Leuk Lymphoma. 2008;49:998–1001.
   PubMed Web of Science ®Google Scholar
• Schlenk RF, Frohling S, Hartmann F, et al. Phase III study of all-trans retinoic acid in previously untreated patients 61 years or older with acute myeloid leukemia. Leukemia. 2004;18:1798–1803.
   PubMed Web of Science ®Google Scholar
• Schlenk RF, Lubbert M, Benner A, et al. All-trans retinoic acid as adjunct to intensive treatment in younger adult patients with acute myeloid leukemia: results of the randomized AMLSG 07-04 study. Ann Hematol. 2016;95:1931–1942.
   PubMed Web of Science ®Google Scholar
• Burnett AK, Hills RK, Green C, et al. The impact on outcome of the addition of all-trans retinoic acid to intensive chemotherapy in younger patients with nonacute promyelocytic acute myeloid leukemia: overall results and results in genotypic subgroups defined by mutations in NPM1, FLT3, and CEBPA. Blood. 2010;115:948–956.
   PubMed Web of Science ®Google Scholar
• Martelli MP, Gionfriddo I, Mezzasoma F, et al. Arsenic trioxide and all-trans retinoic acid target NPM1 mutant oncoprotein levels and induce apoptosis in NPM1-mutated AML cells. Blood. 2015;125:3455–3465.
   PubMed Web of Science ®Google Scholar
• Adedoyin A, Stiff DD, Smith DC, et al. All-trans-retinoic acid modulation of drug-metabolizing enzyme activities: investigation with selective metabolic drug probes. Cancer Chemother Pharmacol. 1998;41:133–139.
   PubMed Web of Science ®Google Scholar
• Luo FR, Yang Z, Camuso A, et al. Dasatinib (BMS-354825) pharmacokinetics and pharmacodynamic biomarkers in animal models predict optimal clinical exposure. Clin Cancer Res. 2006;2:7180–7186.
   Google Scholar
• Demetri GD, Lo Russo P, MacPherson IR, et al. Phase I dose-escalation and pharmacokinetic study of dasatinib in patients with advanced solid tumors. Clin Cancer Res. 2009;15:6232–6240.
   PubMed Web of Science ®Google Scholar
• Dai G, Pfister M, Blackwood-Chirchir A, et al. Importance of characterizing determinants of variability in exposure: application to dasatinib in subjects with chronic myeloid leukemia. J Clin Pharmacol. 2008;48:1254–1269.
   PubMed Web of Science ®Google Scholar
• Boutzen H, Saland E, Larrue C, et al. Isocitrate dehydrogenase 1 mutations prime the all-trans retinoic acid myeloid differentiation pathway in acute myeloid leukemia. J Exp Med. 2016;213:483–497.
   PubMed Web of Science ®Google Scholar