Acute myeloid leukemia (AML) is a malignant and heterogeneous clonal disorder of hematopoietic stem and progenitor cells (HSPCs) with an annual incidence of 3-8/100000. Even the majority of AML patients respond to the initial standard induction chemotherapy, 10-40% of patients do not achieve complete remission and are considered primary refractory disease. Further, relapse is another common scenario in AML treatment and occurs in 40-50% of younger and the great majority of elderly patients. Primary refractory and relapse lead to the lower long-term survival rates of AML and therefore represent the core problem in the treatment of AML. In general, Leukemia stem cells (LSCs), especially in their quiescent state, are often highly resistant to the conventional chemotherapies, leading to the refractory and relapse of the disease. In contrast to the accumulating knowledge about the process of leukemogenesis, molecular mechanisms and biological alterations associated with relapsed/refractory acute myeloid leukemia are still limited.
To achieve long-term remissions and eventually cure leukemia, eliminating the quiescent LSCs is required. The major challenge in targeting LSCs is developing therapies that largely spare hematopoietic stem cells (HSCs) while eradicating LSCs, especially quiescent LSCs. The quiescent LSCs are characterized by their different metabolism states, bone marrow microenvironment, changes in the structure and function of organelles, and genetic and epigenetic alterations. This Research Topic aims to focus on the molecular mechanisms and biological alterations between quiescent LSCs and cycling LSCs, and between LSCs and HSCs, as well as different strategies targeting quiescent LSCs.
Original research articles and review articles are welcome. Preferred subtopics include but are not limited to:
• Mechanisms that maintain LSCs or HSCs survival, self-renewal and quiescence
• Chemical signals, exosomes or physical interactions within microenvironment of LSCs or HSCs
• Studies on altered structure and function of organelles in Relapsed/refractory AML
• Studies on molecular regulation of leukemia progression and chemo-sensitivity
• Function of Splicing factors in normal haematopoiesis and hematopoietic malignancies
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Acute myeloid leukemia (AML) is a malignant and heterogeneous clonal disorder of hematopoietic stem and progenitor cells (HSPCs) with an annual incidence of 3-8/100000. Even the majority of AML patients respond to the initial standard induction chemotherapy, 10-40% of patients do not achieve complete remission and are considered primary refractory disease. Further, relapse is another common scenario in AML treatment and occurs in 40-50% of younger and the great majority of elderly patients. Primary refractory and relapse lead to the lower long-term survival rates of AML and therefore represent the core problem in the treatment of AML. In general, Leukemia stem cells (LSCs), especially in their quiescent state, are often highly resistant to the conventional chemotherapies, leading to the refractory and relapse of the disease. In contrast to the accumulating knowledge about the process of leukemogenesis, molecular mechanisms and biological alterations associated with relapsed/refractory acute myeloid leukemia are still limited.
To achieve long-term remissions and eventually cure leukemia, eliminating the quiescent LSCs is required. The major challenge in targeting LSCs is developing therapies that largely spare hematopoietic stem cells (HSCs) while eradicating LSCs, especially quiescent LSCs. The quiescent LSCs are characterized by their different metabolism states, bone marrow microenvironment, changes in the structure and function of organelles, and genetic and epigenetic alterations. This Research Topic aims to focus on the molecular mechanisms and biological alterations between quiescent LSCs and cycling LSCs, and between LSCs and HSCs, as well as different strategies targeting quiescent LSCs.
Original research articles and review articles are welcome. Preferred subtopics include but are not limited to:
• Mechanisms that maintain LSCs or HSCs survival, self-renewal and quiescence
• Chemical signals, exosomes or physical interactions within microenvironment of LSCs or HSCs
• Studies on altered structure and function of organelles in Relapsed/refractory AML
• Studies on molecular regulation of leukemia progression and chemo-sensitivity
• Function of Splicing factors in normal haematopoiesis and hematopoietic malignancies
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
