4.5 Article

Plasmacytoid Dendritic Cell Infiltration in Acute Myeloid Leukemia

期刊

CANCER MANAGEMENT AND RESEARCH
卷 12, 期 -, 页码 11411-11419

出版社

DOVE MEDICAL PRESS LTD
DOI: 10.2147/CMAR.S260825

关键词

acute myeloid leukemia; AML; tumor-forming plasmacytoid dendritic cells; TF-PDCs; prognosis; hematopoietic stem cell transplantation

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资金

  1. National Natural Science Fund [81600166, 81873424]
  2. Science and Technology Innovation Promotion Project of AMU [2019XLC3020]
  3. Project of Key Laboratory of Tumor Immunopathology
  4. Ministry of Education of China [2018jsz102]

向作者/读者索取更多资源

Introduction: Increasing evidence has demonstrated that plasmacytoid dendritic cells (PDCs) in the tumor microenvironment (TME) play an important role in tumorigenesis and progression. PDC infiltration has been found in certain malignancies such as classic Hodgkin's lymphoma and chronic myelomonocytic leukemia. Our previous work reported that PDC infiltration could occur in acute myeloid leukemia (AML), but the clinical significance of PDC in AML has not been thoroughly investigated. Patients and Methods: Here, we evaluated the clinical significance of PDC to AML transition in a leukemia microenvironment. The frequency of PDCs in 80 acute myelomonocytic leukemia (AML-M4) and 83 acute monocytic leukemia (AML-M5) patients was determined by flow cytometry. Results: We found 62 cases with PDC infiltration. These patients showed higher numbers of bone marrow blasts, higher mean Hb concentration, and required more cycles of chemotherapy before achieving complete remission (CR), but had lower white blood cell and platelet counts compared to patients without PDC infiltration. Drug sensitivity analysis showed that patients with PDC infiltration had lower sensitivity to standard chemotherapy regimens. Kaplan-Meier survival curves demonstrated that patients with PDC infiltration had a shorter overall survival (OS) time and progression-free survival time. Discussion: These results suggested that PDC infiltration can be used for risk stratification of AML-M4/M5, and PDCs may transdifferentiate into leukemia in an AML microenvironment.

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