This case demonstrates that durable responses can occur upon retreatment with decitabine.

Clinical studies have demonstrated that decitabine has activity in patients with MDS.

The main adverse reaction of decitabine was myelosuppression, infection and so on.

Patients continued to receive decitabine until disease progression or an unacceptable adverse event occurred.

The clinical data of 12 MDS and AML patients treated with decitabine were analyzed retrospectively.

Induction of CTA expression sufficient for recognition by T-cells occurs in AML patients receiving decitabine.

Most of patients well tolerate the adverse effects of decitabine after active symptomatic and supportive treatment.

This protection can be reversed without increasing myelotoxicity by combining tetrahydrouridine with a lower dose of decitabine.

He was retreated with decitabine and again achieved a CR, which has been maintained for 6 months.

We investigated the efficacy and toxicity of the hypomethylating agent decitabine as initial therapy in older patients with AML.

Peripheral blood blasts serially isolated from AML patients treated with decitabine were evaluated for CTA gene expression and demethylation.

Although effective, the complete response rate to decitabine is only around 30% and the overall survival remains poor.

Response was evaluated after four and six cycles; patients responding at the end of six cycles could continue treatment with decitabine.

We hypothesize that defining how decitabine influences the immune responses in AML will facilitate the development of novel immune-based leukaemia therapeutics.

T-cell expression of inhibitory molecules was upregulated and the ability of CD8 T cells to produce cytokines was decreased upon decitabine treatment.

Collectively, our study suggests that immune-based analyses may predict clinical response to decitabine and provide a therapeutic strategy to improve the treatment of AML.