Abstract

Hypomethylating agents (HMAs) are effective therapies in myelodysplastic syndromes (MDS), but allogeneic hematopoietic stem cell transplantation (allo-HSCT) is the only way to cure MDS. According to the current literature, it is difficult to confirm whether HMAs bridging therapy is beneficial for MDS patients receiving allo-HSCT. Therefore, we tried to evaluate the effect of HMAs on long-term survival of the MDS patients. Databases, including PubMed, Embase Ovid, and the Cochrane Library, were searched for studies published up to January 10, 2021. Patients who accepted HMAs bridging to allo-HSCT were defined as experimental group, while patients who received the best supportive care (BSC) before allo-HSCT were control group. Overall survival (OS) was the primary end point. Seven studies were included in the final analysis. The final results showed no OS differences between patients accepted HMAs before allo-HSCT and those received BSC (HR = 0.86, 95% CI: 0.64–1.15, p = 0.32), indicating that MDS patients' long-term survival did not benefit from HMAs bridging therapy before allo-HSCT. This conclusion needs to be further verified by a large number of prospective randomized controlled trials, which have guiding significance for the treatment of MDS patients.

Highlights

  • Myelodysplastic syndrome (MDS) is a group of heterogeneous clonal diseases originated from hematopoietic stem cells and characterized by myelodysplasia

  • The inclusion and exclusion criteria were as follows: (1) this study focused on the effect of Hypomethylating agents (HMAs) on the prognosis of MDS patients before allo-HSCT; (2) in this study, bridging treatments before transplantation were HMAs and best supportive care (BSC); (3) sufficient clinical data were provided in this study, at least the Overall survival (OS); and (4) the hazard ratio (HR) and its 95% confidence interval were directly reported, or calculated from raw data; (5) the study was published in full in English; (6) the study included human subjects; (7) the article was not a review, case report or animal study

  • After 68 repetitions were eliminated, 289 citations were screened for titles and abstracts, of which 254 citations irrelevant results, the final 7 studies were included in the meta-analysis[21–27]

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Summary

Introduction

Myelodysplastic syndrome (MDS) is a group of heterogeneous clonal diseases originated from hematopoietic stem cells and characterized by myelodysplasia. Its clinical manifestations include anemia, infection and hemorrhage caused by hemocytopenia, and variable risk progressed to acute myeloid leukemia (AML). Recent studies have shown that epigenetic changes, especially abnormal DNA methylation, are important factors leading to the occurrence and development of MDS [1–3]. HMAs, azacitidine (AZA) and decitabine (DEC), have been approved by FDA for MDS treatment since 2004. The inhibition of DNA methyltransferase by HMAs is thought to be responsible for the hypomethylation and reactivation of tumor suppressor genes, inducing the terminal differentiation and apoptosis of neoplastic cells, which may contribute to improvements in allo-HSCT outcome by a reduction in tumor burden.

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