cells Article Aberrant Bone Homeostasis in AML Is Associated with Activated Oncogenic FLT3-Dependent Cytokine Networks 1, 2, 3 3,4 5, Isabel Bär y, Volker Ast y, Daria Meyer , Rainer König , Martina Rauner z, 5, , 1, , Lorenz C. Hofbauer * z and Jörg P. Müller * z 1 Institute of Molecular Cell Biology, Center for Molecular Biomedicine (CMB), Jena University Hospital, 07745 Jena, Germany;
[email protected] 2 Institute for Clinical Chemistry, Medical Faculty Mannheim, Heidelberg University, 69117 Heidelberg, Germany;
[email protected] 3 Center for Infectious Diseases and Infection Control, Jena University Hospital, 07745 Jena, Germany;
[email protected] (D.M.);
[email protected] (R.K.) 4 Integrated Research and Treatment Center, Center for Sepsis Control and Care (CSCC), 07745 Jena, Germany 5 Department of Medicine III & Center for Healthy Aging, Technical University Dresden, 01069 Dresden, Germany;
[email protected] * Correspondence:
[email protected] (L.C.H.);
[email protected] (J.P.M.); Tel.: +49-351-458-3173 (L.C.H.); +49-364-1939-5634 (J.P.M.) These authors joined first. y These authors equally contributed. z Received: 5 October 2020; Accepted: 5 November 2020; Published: 9 November 2020 Abstract: Acute myeloid leukaemia (AML) is a haematopoietic malignancy caused by a combination of genetic and epigenetic lesions. Activation of the oncoprotein FLT3 ITD (Fms-like tyrosine kinase with internal tandem duplications) represents a key driver mutation in 25–30% of AML patients. FLT3 is a class III receptor tyrosine kinase, which plays a role in cell survival, proliferation, and differentiation of haematopoietic progenitors of lymphoid and myeloid lineages.