Levis Mark, Pham Rosalyn, Smith B Douglas, Small Donald
Department of Oncology, Baltimore, MD 21231, USA.
Blood. 2004 Aug 15;104(4):1145-50. doi: 10.1182/blood-2004-01-0388. Epub 2004 May 4.
Patients with acute myeloid leukemia (AML) harboring internal tandem duplication mutations of the FLT3 receptor (FLT3/ITD mutations) have a poor prognosis compared to patients lacking such mutations. Incorporation of FLT3 inhibitors into existing chemotherapeutic regimens has the potential to improve clinical outcomes in this high-risk group of patients. CEP-701, an indolocarbazole-derived selective FLT3 inhibitor, potently induces apoptosis in FLT3/ITD-expressing cell lines and primary leukemic blasts. We conducted a series of in vitro cytotoxicity experiments combining CEP-701 with chemotherapy using the FLT3/ITD-expressing cell lines MV4-11 and BaF3/ITD as well as a primary blast sample from a patient with AML harboring a FLT3/ITD mutation. CEP-701 induced cytotoxicity in a synergistic fashion with cytarabine, daunorubicin, mitoxantrone, or etoposide if used simultaneously or immediately following exposure to the chemotherapeutic agent. In contrast, the combination of pretreatment with CEP-701 followed by chemotherapy was generally antagonistic, particularly with the more cell cycle-dependent agents such as cytarabine. This effect appears to be due to CEP-701 causing cell cycle arrest. We conclude that in FLT3/ITD-expressing leukemia cells, CEP-701 is synergistic with standard AML chemotherapeutic agents, but only if used simultaneously with or immediately following the chemotherapy. These results should be considered when designing trials combining chemotherapy with each of the FLT3 inhibitors currently in clinical development.
与缺乏此类突变的患者相比,携带FLT3受体内部串联重复突变(FLT3/ITD突变)的急性髓系白血病(AML)患者预后较差。将FLT3抑制剂纳入现有化疗方案有可能改善这一高危患者群体的临床结局。CEP-701是一种吲哚咔唑衍生的选择性FLT3抑制剂,可有效诱导表达FLT3/ITD的细胞系和原发性白血病细胞凋亡。我们使用表达FLT3/ITD的细胞系MV4-11和BaF3/ITD以及来自一名携带FLT3/ITD突变的AML患者的原发性白血病细胞样本,进行了一系列将CEP-701与化疗联合的体外细胞毒性实验。如果同时使用或在接触化疗药物后立即使用,CEP-701与阿糖胞苷、柔红霉素、米托蒽醌或依托泊苷以协同方式诱导细胞毒性。相比之下,先用CEP-701预处理再进行化疗的联合方案通常具有拮抗作用,尤其是对于阿糖胞苷等更依赖细胞周期的药物。这种效应似乎是由于CEP-701导致细胞周期停滞。我们得出结论,在表达FLT3/ITD的白血病细胞中,CEP-701与标准AML化疗药物具有协同作用,但前提是与化疗同时使用或在化疗后立即使用。在设计将化疗与目前正在临床开发的每种FLT3抑制剂联合的试验时,应考虑这些结果。