[1] PATEL J P, GÖNEN M, FIGUEROA M E, et al. Prognostic relevance of integrated genetic profiling in acute myeloid leukemia[J]. N Engl J Med, 2012, 366(12):1079-1089. [2] PAPAEMMANUIL E, GERSTUNG M, BULLINGER L, et al. Genomic classification and prognosis in acute myeloid leukemia[J]. N Engl J Med, 2016, 374(23):2209-2221. [3] PASIC I,DA'NA W,LAM W,et al. Influence of FLT3-ITD and NPM1 status on allogeneic hematopoietic cell transplant outcomes in patients with cytogenetically normal AML[J]. Eur J Haematol,2019,102(4):368-374. [4] MARCUCCI G, MAHARRY K S, METZELER K H, et al. Clinical role of microRNAs in cytogenetically normal acute myeloid leukemia:miR-155 upregulation independently identifies high-risk patients[J]. J Clin Oncol, 2013, 31(17):2086-2093. [5] GERLOFF D,GRUNDLER R,WURM A A,et al. NF-κB/STAT5/miR-155 network targets PU.1 in FLT3-ITD-driven acute myeloid leukemia[J]. Leukemia,2015,29(3):535-547. [6] KHALIFE J,RADOMSKA H S,SANTHANAM R,et al. Pharmacological targeting of miR-155 via the NEDD8-activating enzyme inhibitor MLN4924(Pevonedistat) in FLT3-ITD acute myeloid leukemia[J]. Leukemia,2015,29(10):1981-1992. [7] YOON Y,KIM YO,LIM NY,et al. Shikonin, an ingredient of Lithospermum erythrorhizon induced apoptosis in HL60 human premyelocytic leukemia cell line[J]. Planta Med,1999,65(6):532-535. [8] MAO X,YU C R,LI W H,et al. Induction of apoptosis by shikonin through a ROS/JNK-mediated process in Bcr/Abl-positive chronic myelogenous leukemia (CML) cells[J]. Cell Res,2008,18(8):879-888. [9] ZHAO Q L, ASSIMOPOULOU A N, KLAUCK S M, et al. Inhibition of c-MYC with involvement of ERK/JNK/MAPK and AKT pathways as a novel mechanism for shikonin and its derivatives in killing leukemia cells[J]. Oncotarget, 2015, 6(36):38934-38951. [10] KOTTARIDIS P D,GALE R E,FREW M E,et al. The presence of a FLT3 internal tandem duplication in patients with acute myeloid leukemia (AML) adds important prognostic information to cytogenetic risk group and response to the first cycle of chemotherapy:analysis of 854 patients from the United Kingdom Medical Research Council AML 10 and 12 trials[J]. Blood,2001,98(6):1752-1759. [11] THIEDE C,STEUDEL C,MOHR B,et al. Analysis of FLT3-activating mutations in 979 patients with acute myelogenous leukemia:association with FAB subtypes and identification of subgroups with poor prognosis[J]. Blood,2002,99(12):4326-4335. [12] FRÖHLING S, SCHLENK R F, BREITRUCK J, et al. Prognostic significance of activating FLT3 mutations in younger adults (16 to 60 years) with acute myeloid leukemia and normal cytogenetics:A study of the AML Study Group Ulm[J]. Blood, 2002, 100(13):4372-4380. [13] SCHMID C,LABOPIN M,SOCIÉ G,et al. Outcome of patients with distinct molecular genotypes and cytogenetically normal AML after allogeneic transplantation[J]. Blood,2015,126(17):2062-2069. [14] SONG Y, MAGENAU J, LI Y M, et al. FLT3 mutational status is an independent risk factor for adverse outcomes after allogeneic transplantation in AML[J]. Bone Marrow Transplant, 2016, 51(4):511-520. [15] DEOL A,SENGSAYADETH S,AHN K W,et al. Does FLT3 mutation impact survival after hematopoietic stem cell transplantation for acute myeloid leukemia? A Center for International Blood and Marrow Transplant Research (CIBMTR) analysis[J]. Cancer,2016,122(19):3005-3014. [16] CANAANI J,LABOPIN M,HUANG X J,et al. T-cell replete haploidentical stem cell transplantation attenuates the prognostic impact of FLT3-ITD in acute myeloid leukemia:A report from the Acute Leukemia Working Party of the European Society for Blood and Marrow Transplantation[J]. Am J Hematol,2018,93(6):736-744. [17] ZHANG Y Y,MO X D,ZHANG X H,et al. FLT3 internal tandem duplication does not impact prognosis after haploidentical allogeneic hematopoietic stem cell transplantation in AML patients[J]. Bone Marrow Transplant,2019,54(9):1462-1470. [18] LARROSA-GARCIA M, BAER M R. FLT3 inhibitors in acute myeloid leukemia:current status and future directions[J]. Mol Cancer Ther, 2017, 16(6):991-1001. [19] STONE R M, MANDREKAR S J, SANFORD B L, et al. Midostaurin plus chemotherapy for acute myeloid leukemia with a FLT3 mutation[J]. N Engl J Med, 2017, 377(5):454-464. [20] XU L H,GUO Y,CEN J N,et al. Overexpressed miR-155 is associated with initial presentation and poor outcome in Chinese pediatric acute myeloid leukemia[J]. Eur Rev Med Pharmacol Sci, 2015,19(24):4841-4850. [21] RAMAMURTHY R, HUGHES M, MORRIS V, et al. MiR-155 expression and correlation with clinical outcome in pediatric AML:A report from Children's Oncology Group[J]. Pediatr Blood Cancer, 2016, 63(12):2096-2103. [22] ANDUJAR I,RECIO M C,BACELLI T,et al. Shikonin reduces oedema induced by phorbol ester by interfering with IkappaBalpha degradation thus inhibiting translocation of NF-kappaB to the nucleus[J]. Br J Pharmacol,2010,160(2):376-388. [23] CHENG Y W,CHANG C Y,LIN K L,et al. Shikonin derivatives inhibited LPS-induced NOS in RAW 264.7 cells via downregulation of MAPK/NF-kappaB signaling[J]. J Ethnopharmacol,2008, 120(2):264-271. [24] ANDUJAR I,RÍOS J L,GINER R M,et al. Pharmacological properties of shikonin-a review of literature since 2002[J]. Planta Med,2013,79(18):1685-1697. [25] SU L,LIU L H,WANG Y L,et al. Long-term systemic toxicity of shikonin derivatives in Wistar rats[J]. Pharm Biol,2013,52(4):486-490. |