Acute myeloid leukemia (AML) is a common type of leukemia in adults, and according to preliminary statistics in China in 2010, there were nearly 16,000 new cases of leukemia annually, of which more than 50% were AML (non-acute o young granulocytic leukemia). AML is more common in the elderly, with about 14,500 new cases of AML per year in the United States over the age of 60, of which 1/3 are over 75 years old, and about In Europe, there are about 18,000 new cases per year. The world population has been gradually aging, and the population survey in Jiangsu Province at the end of 2012, 18.89% of the total population is over 60 years old. The incidence of AML in the elderly is increasing year by year, and therefore the basic disease characteristics and treatment of AML in the elderly are receiving increasing attention. Advanced age is one of the most common factors for the poor prognosis of AML, with survival decreasing with each 10-year span above the age of 40 years, and only 10% of elderly AML surviving beyond 2 years. Compared to younger AML, older AML not only has factors associated with poor prognosis (physical status, organ insufficiency, and comorbidities), but also its specific cell biology, such as often secondary to myelodysplastic syndromes (MDS), often with complex karyotypes and monosomal karyotypes, and significantly higher expression of multidrug resistance genes, while karyotypes with good prognosis, such as t(8;21), inv(16) and NPM1 mutations are rare. There is no universally applicable standard regimen for elderly AML, and studies often report controversial results, for example, some authors attribute the poor prognosis of elderly AML to the lack of intense chemotherapy, while others argue that intense chemotherapy prolongs survival but subsequently reduces the quality of survival compared with palliative treatment. Sweden reported clinical data on 2767 elderly AML cases collected from 1997 to 2005, and intense chemotherapy showed only a mild improvement in overall survival over palliative treatment. Age is one of the key factors influencing the choice of treatment regimen. For elderly AML aged 60 to 69 years, investigators generally agree that the vast majority of patients can tolerate standard treatment, including a subset of patients who can receive allogeneic hematopoietic stem cell transplantation (allo-HSCT). For example, Kantarjian et al. in the United States concluded that AML in elderly patients ≥ 70 years of age had a poor prognosis with an 8-week mortality rate of ≥ 30% and a median survival of < 6 months, so this group of AML could not benefit from intense chemotherapy. In contrast, Juliusson et al. in Sweden held the opposing view that the mortality rate within 8 weeks of intense chemotherapy in elderly AML aged 70-79 years with a physical status of 0-II was only 8%, and the 2-year survival rates of patients with non-secondary (de novo) and secondary AML were about 35% and 5%, respectively, so most AML patients aged 70-79 years could benefit from intense chemotherapy. There is no unified objective criterion to determine whether patients can tolerate intense chemotherapy, but studies have shown that the "3+7" regimen of cytarabine combined with anthracyclines in AML aged 60-65 years with good physical status (0-1) and good karyotype can result in long survival and is the best treatment option. However, the number of patients in this subgroup is extremely limited, and the number of patients in this subgroup is very high. the country, the number of elderly AML receiving intense chemotherapy is low, taking into account patient fitness, comorbidities, and nutrition. More than 2/3 of elderly AML patients opted for supportive therapy in the early 1990s, with a median survival of only 1 month. Low-dose cytarabine only prolonged survival by 1 month compared to hydroxyurea treatment, and neither survival nor CR rates were improved in elderly AML patients with poor karyotype. Domestic and international scholars continue to investigate new regimens to improve long-term patient survival while reducing treatment-related side effects, such as the new drugs gituximab (GO), clofarabine, 5-azacitidine, and decitabine. GO monotherapy for first-episode elderly AML resulted in a CR rate of up to 25%, but given data from a phase III clinical trial enrolling 637 young patients with first-episode AML from August 2004 to August 2009, it was found that GO did not improve CR rates, disease-free survival, or overall survival of patients, and considering the side effects of GO, GO was withdrawn from the market in 2010. Based on the results of a multicenter clinical trial, the National Comprehensive Cancer Network (NCCN) recently proposed clofarabine, 5-azacitidine and decitabine as alternative treatment options for AML in the elderly. Clofarabine and 5-azacytidine are not yet available in China, so the focus of domestic scholars is decitabine alone or in combination with low-dose chemotherapy for elderly AML. Decitabine (5-aza-2'-deoxycytidine) is a cytosine analogue, first synthesized by Pliml and Sorm in the early 1960s. In tumor cells, decitabine is phosphorylated by deoxycytidine kinase and doped to DNA as a phosphate. High concentrations of decitabine adulteration inhibit DNA synthesis to induce cell death and exert its cytotoxic effects; low concentrations of decitabine adulteration can replace cytosine in tumor cells by covalent binding to DNA methyltransferase (DNMT), which inactivates DNA methyltransferase without causing cell death. Decitabine induces differentiation of tumor cells to normal cells or induces apoptosis of tumor cells by reversing the DNA methylation process. The dose of decitabine has been continuously explored by clinical investigators. Early clinical trials used high doses of decitabine (total dose up to ~1000 mg/m2 per cycle) alone or in combination with anthracyclines, resulting in high hematologic and non-hematologic toxicity, and in the 1980s, after recognizing that the mechanism of action of low-dose decitabine was hypomethylation and promotion of tumor cell differentiation without damage to normal hematopoietic stem cells, clinical trials of phase I-III decitabine were born. . Firstly, the phase I clinical trial reported in 2004 investigated the efficacy and safety of different low doses of decitabine (5, 10, 15 or 20 mg/m2/d for 10-20 days) for the treatment of malignant hematological diseases, and the results showed that decitabine 15 mg/m2/d x 10 days was the most effective regimen with a response rate of 65% and good tolerability. Also based on the efficacy and good safety profile of a 5-day regimen of decitabine 20 mg/m2/d in MDS, a phase II clinical trial at the University of Washington used a 5-day regimen of decitabine 20 mg/m2/d in 55 elderly AML patients with high-risk primary treatment (median age 74 years, intermediate or high-risk karyotype, 42% secondary AML, median bone marrow primitive cells 50%) for a median of 3 cycles of decitabine. bin, 25% overall response rate, 29% stable disease, median survival of 7.7 months, median survival of 14 months for responders, 7% mortality within 30 days, and good safety profile. Surprisingly those patients with AML with high-risk karyotypes had the same response rate and some patients eventually achieved complete cytogenetic remission, which is extremely rare with low-dose cytarabine treatment, unfortunately this subgroup of patients was not stratified in the phase III clinical study. Good trial results and tolerability have opened the platform for later phase III clinical trials on decitabine dosing.Kantarjian et al. reported the results of a randomized open multicenter phase III clinical trial in primary elderly AML with the aim of evaluating the pros and cons of low-dose decitabine versus low-dose cytarabine or supportive therapy.The study enrolled 632 elderly primary AML patients over 65 years of age, and the results of the decitabine alone The group had a slightly longer survival (7.7 months vs. 5.0 months) than the selective treatment group (low-dose cytarabine or supportive therapy). Investigators have reported phase I clinical trials of decitabine in combination with other drugs for AML, and Scandura et al. explored different doses of decitabine (total doses of 60 mg/m2, 100 mg/m2 and 140 mg/m2) in combination with DA for AML, with no increase in overall adverse effects compared to DA alone. DNA hypomethylation was observed in CD34+ bone marrow cells in different subgroups, while DNA hypomethylation tended to be most pronounced with decitabine 20 mg/m2 × 3 days. Considering the more pronounced adverse effects of decitabine 20 mg/m2×7 days, the authors suggested that subsequent phase II clinical trials could use the combination of decitabine (20 mg/m2×5 days). While other phase I clinical trials of decitabine (20 mg/m2/d for 5 days) combination therapy for AML have confirmed the good safety of this dose. yang et al. treated leukemia patients with different doses of decitabine (5 mg/m2/d, 10 mg/m2/d, 15 mg/m2/d, 20 mg/m2/d and 100 mg/m2/d) and monitored DNA hypomethylation status, and found that LINE gene methylation decreased from 70.2% to 71.4%, 62.8%, 60.1%, 59.4% and 55.7%, respectively, showing a dose-dependent decrease curve. Our scholars often use reduced-dose chemotherapy regimens to treat elderly AML, such as the CAG regimen (a 14-day regimen of G-CSF, low-dose cytarabine combined with low-dose aclarubicin) has been widely used in elderly AML, and the efficacy and tolerability have shown good, and we have previously reported that elderly AML patients benefit from the CAG regimen. We have previously reported that elderly AML patients benefited from the CAG regimen, but an age-stratified analysis found that survival was not prolonged in elderly AML patients over 70 years of age, and the beneficiaries were mainly patients aged 60 to 69 years. From the results of several reports, it is clear that the efficacy of CAG is higher than that of decitabine alone. How to increase the efficacy without increasing the cytotoxic effect of the treatment regimen has been explored by scholars in China and abroad. The main mechanism of action of low-dose decitabine is to promote cell differentiation and hypomethylation. Can the combination of low-dose cytotoxic drugs for the treatment of elderly AML achieve the goal of increasing efficacy without increasing toxicity?