Acute myeloid leukemia (AML) is an aggressive bone marrow disease. Despite advances in treatment, AML remains a therapeutic challenge due to high rates of disease relapse. Many factors contribute to disease relapse including apoptotic dysregulation, genetic mutations, and the bone marrow microenvironment (BMM). The BMM consisting of cells, extracellular matrix and secretory factors sustain normal hematopoiesis but undergoes overhauling in AML to support leukemia. For instance, CXCR4/CXCL12, VLA-4/VCAM-1, CD44 interactions are involved in mediating resistance to standard chemotherapy in AML.

AML is a heterogenous disease. This heterogeneity accounts for difference in response to chemotherapy as it affects the AML cells inherent chemoresistance potential. Studies have shown reduced chemosensitivity of AML in co-culture studies highlighting the role of niche in imparting chemoprotection. This emphasizes the need to identify BMM factors (such as protein or miRNA or lncRNA) involved in desensitizing cells to chemotherapeutic drugs. It is not necessary that one such factor will be effective across all subtypes of AML, and thus, factors exclusive for different mutations in AML might be needed. Despite intensive research in the area, no definitive therapeutic solutions currently exist to overcome niche-induced drug resistance in AML.

Scope and information for authors includes manuscript types like Original research, brief research report, review, mini review and perspective covering, but not limited to, the following sub-topics are welcome:
• Bone marrow niche derived factors imparting chemoresistance
• AML derived molecular factors remodeling the bone marrow niche for support
• Role of different bone marrow niche cells in protecting AML against
• chemotherapeutic drugs
• Targeting niche to overcome AML chemoresistance
• Clinico-therapeutic implications of niche-induced chemoresistance in AML

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Niche-induced chemoprotection in acute myeloid leukemia