In this study, we evaluated the efficacy and toxicity of DCAG, relative to the standard dose chemotherapy regimen (IA), for patients with newly diagnosed AML, aged 14–60 years. The modifications included that the dose of cytarabine was increased to 100 mg/m2 q12 hrs for 5 days and aclarubicin hydrochloride was increased to 20 mg/m2 for 5 days. (For elderly patients with AML, the standard dosages of cytarabine and aclarubicin hydrochloride are 10 mg/m2 q12 hrs and 10 mg/day, respectively, each for 5 days.)

The primary objective of this study was to determine whether induction therapy with DCAG resulted in similar remission rates, OS, or event-free survival (EFS) compared the IA regimen. Additionally, clinical features or molecular markers were investigated that may predict the response of patients with AML to DCAG, and may differentiate those patients who are more likely to respond to DCAG.


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The review board of Chinese PLA General Hospital approved all the study procedures, and the informed consent forms, in accordance with the Declaration of Helsinki.


Between April 2012 and September 2017, 161 consecutive patients with AML were enrolled in this study (Table 1). Among these patients, 97 received IA induction chemotherapy, with idarubicin and cytarabine for 7 days. DCAG was administrated to the other 64 patients.

(To view a larger version of Table 1, click here.)

All these patients received diagnoses of AML (not including acute promyelocytic leukemia) based on criteria of the French-American-British and World Health Organization,1,5 and all patients provided written informed consent.

At diagnosis, bone marrow was obtained from each patient, and chromosomal analysis and immunophenotyping were conducted. The following molecular markers were analyzed: AML1-ETO, PML (promyelocytic leukemia)/RARA (retinoic acid receptor alpha), NPM1 (nucleophosmin 1), CBFB (core-binding factor beta)/MYH11 (myosin heavy chain 11), and MLL PTD (partial tandem duplication). Patients with AML1-ETO, PML/RARA, CBFB/MYH11, and/or NPM1 without FLT3 (FMS-like tyrosine kinase receptor 3)-ITD (internal tandem duplication) were defined as favorable-risk in accordance with the NCCN (National Comprehensive Cancer Network) AML risk status evaluation. Patients with the following were considered poor-risk: complex karyotypes, unfavorable cytogenetics, FLT3-ITD gene expression, or TP53 mutation. Other patients were classified as intermediate-risk.


We retrospectively studied 161 patients with AML who received induction chemotherapy (DCAG or IA induction chemotherapy). The treatment choice was based on patient wishes, as policy. Specifically, 97 patients received IA induction chemotherapy, with idarubicin (10–12 mg/m2) for 3 days and cytarabine (100 mg/m2, every 12 hrs) for 7 days. Another 64 patients received a DCAG regimen: decitabine 20 mg/m2, days 1–5; aclarubicin 20 mg/m2, days 1–5; cytarabine 100 mg/m2, every 12 hrs, days 1–5; and granulocyte colony-stimulating factor 300 μg/day subcutaneously from day 0 to the time of neutrophil recovery.

Consolidation chemotherapy was administered to 56 patients in the DCAG group and 89 patients in the IA induction chemotherapy group, consisting of the following: conventional dose of cytarabine and anthracycline, or mitoxantrone; or middle-to-high-dose cytarabine; or hematopoietic stem cell transplantation. Among them, the patients who received >2 cycles of consolidation chemotherapy were used for the survival analysis.

Routine blood count, liver function, and electrolyte and creatinine levels were recorded twice each week. Adverse events, concomitant medications, and clinical laboratory analyses were recorded weekly. The treatment continued until any of the following occurred: disease progression, intolerable toxicity, death, loss to follow-up, abandonment of treatment, or withdrawal of consent to further treatment. All patients received supportive care in accordance with institutional practices, including blood product transfusions and prophylactic or symptomatic use of anti-infective agents and cytokines, and other therapies appropriate for the symptomatic treatment of AML and its complications.

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