1) Stirewalt DL, Radich JP. The role of FLT3 in haematopoietic malignancies. Nat Rev Cancer. 2003; 3: 650-65
|
|
|
2) Kiyoi H, Naoe T. Biology, clinical relevance, and molecularly targeted therapy in acute leukemia with FLT3 mutation. Int J Hematol. 2006; 83: 301-8
|
|
|
3) Swerdlow S, Campo E, Harris N, et al. In: WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues, 4th ed. Lyon: IARC Press; 2008
|
|
|
4) Kiyoi H, Yanada M, Ozekia K. Clinical significance of FLT3 in leukemia. Int J Hematol. 2005; 82: 85-92
|
|
|
5) DeAngelo DJ, Stone RM, Heaney ML, et al. Phase 1 clinical results with tandutinib (MLN518), a novel FLT3 antagonist, in patients with acute myelogenous leukemia or high-risk myelodysplastic syndrome: safety, pharmacokinetics, and pharmacodynamics. Blood. 2006; 108: 3674-81
|
|
|
6) Knapper S, Burnett AK, Littlewood T, et al. A phase 2 trial of the FLT3 inhibitor lestaurtinib (CEP701) as first line treatment for older patients with acute myeloid leukemia not considered fit for intensive chemotherapy. Blood. 2006; 108: 3262-70
|
|
|
7) Weisberg E, Boulton C, Kelly LM, et al. Inhibition of mutant FLT3 receptors in leukemia cells by the small molecule tyrosine kinase inhibitor PKC412. Cancer Cell. 2002; 1: 433-43
|
|
|
8) Fiedler W, Serve H, Dohner H, et al. A 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 disease. Blood. 2005; 105: 986-93
|
|
|
9) Zarrinkar PP, Gunawardane RN, Cramer MD, et al. AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML). Blood. 2009; 114: 2984-92
|
|
|
10) Wilhelm SM, Carter C, Tang L, et al. BAY 43-9006 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: 7099-109
|
|
|
11) 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: 184-98
|
|
|
12) Metzelder S, Wang Y, Wollmer E, et al. Compassionate use of sorafenib in FLT3-ITD-positive acute myeloid leukemia: sustained regression before and after allogeneic stem cell transplantation. Blood. 2009; 113: 6567-71
|
|
|
13) Ravandi F, Cortes JE, Jones D, et al. Phase I/II study of combination therapy with sorafenib, idarubicin, and cytarabine in younger patients with acute myeloid leukemia. J Clin Oncol. 2010; 28: 1856-62
|
|
|
14) Johnston SR. Farnesyl transferase inhibitors: a novel targeted tnerapy for cancer. The Lancet Oncology. 2001; 2: 18-26
|
|
|
15) Blum R, Kloog Y. Tailoring Ras-pathway-inhibitor combinations for cancer therapy. Drug Resist Update. 2005; 8: 369-80
|
|
|
16) Lancet JE, Karp JE. Farnesyltransferase inhibitors in hematologic malignancies: new horizons in therapy. Blood. 2003; 102: 3880-9
|
|
|
17) Morgan MA, Ganser A, Reuter CW. Therapeutic efficacy of prenylation inhibitors in the treatment of myeloid leukemia. Leukemia. 2003; 17: 1482-98
|
|
|
18) Rowinsky EK, Windle JJ, Von Hoff DD. Ras protein farnesyltransferase: A strategic target for anticancer therapeutic development. J Clin Oncol. 1999; 17: 3631-52
|
|
|
19) Graaf MR, Richel DJ, van Noorden CJ, et al. Effects of statins and farnesyltransferase inhibitors on the development and progression of cancer. Cancer Treat Rev. 2004; 30: 609-41
|
|
|
20) Harousseau JL. Farnesyltransferase inihibitors in hematologic malignancies. Blood Rev. 2007; 21: 173-82
|
|
|
21) 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: 3361-9
|
|
|
22) Harousseau JL, Lancet JE, Reiffers J, et al. A phase 2 study of the oral farnesyltransferase inhibitor tipifarnib in patients with refractory or relapsed acute myeloid leukemia. Blood. 2007; 109: 5151-6
|
|
|
23) Lancet JE, Gojo I, Gotlib J, et al. A phase 2 study of the farnesyltransferase inhibitor tipifarnib in poor-risk and elderly patients with previously untreated acute myelogenous leukemia. Blood. 2007; 109: 1387-94
|
|
|
24) Karp JE, Flatten K, Feldman EJ, et al. Active oral regimen for elderly adults with newly diagnosed acute myelogenous leukemia: a preclinical and phase 1 trial of the farnesyltransferase inhibitor tipifarnib(R115777, Zarnestra)combined with etoposide. Blood. 2009; 113: 4841-52
|
|
|
25) Karp JE, Smith BD, Gojo I, et al. Phase II trial of tipifarnib as maintenance therapy in first complete remission in adults with acute myelogenous leukemia and poor-risk features. Clin Cancer Res. 2008; 14: 3077-82
|
|
|
26) Ravoet C, Mineur P, Robin V, et al. Farnesyl transferase inhibitor (lonafarnib) in patients with myelodysplastic syndrome or secondary acute myeloid leukaemia: a phase II study. Ann Hematol. 2008; 87: 881-5
|
|
|
27) Cortes J, Faderl S, Estey E, et al. Phase I study of BMS-214662, a farnesyltransferase inhibitor in patients with acute leukemias and high-risk myelodysplastic syndromes. J Clin Oncol. 2005; 23: 2805-12
|
|
|
28) Braun T, Fenaux P. Farnesyltransferase inhibitors and their potential role in therapy for myelodysplastic syndromes and acute myeloid leukaemia. Br J Haematol. 2008; 141: 576-86
|
|
|
29) Raponi M, Harousseau JL, Lancet JE, et al. Identification of molecular predictors of response in a study of tipifarnib treatment in relapsed and refractory acute myelogenous leukemia. Clin Cancer Res. 2007; 13: 2254-60
|
|
|
30) van der Weide K, de Jonge-Peeters SD, Kuipers F, et al. Combining simvastatin with the farnesyl-transferase inhibitor tipifarnib results in an enhanced cytotoxic effect in a subset of primary CD34+ acute myeloid leukemia samples. Clin Cancer Res. 2009; 15: 3076-83
|
|
|
31) Raponi M, Lancet JE, Fan H, et al. A 2-gene classifier for predicting response to the farnesyl-transferase inhibitor tipifarnib in acute myeloid leukemia. Blood. 2008; 111: 2589-96
|
|
|
32) Nagai T, Ohmine K, Fujiwara S, et al. Combination of tipifarnib and rapamycin synergistically inhibits the growth of leukemia cells and overcomes resistance to tipifarnib via alteration of cellular signaling pathways. Leuk Res. 2010; 34: 1057-63
|
|
|