Ioanna Mosialou

TL;DR: It is demonstrated that genetic alterations in osteoblasts can induce acute myeloid leukaemia, identify molecular signals leading to this transformation and suggest a potential novel pharmacotherapeutic approach to acuteMyeloidLeukaemia.

TL;DR: Results identify LCN2 as a bone-derived hormone with metabolic regulatory effects, which suppresses appetite in a MC4R-dependent manner, and show that the control of appetite is an endocrine function of bone.

TL;DR: The notion that osteoblasts are necessary for glucose homeostasis and energy expenditure is strengthened and it is suggested that in addition to osteocalcin, other osteoblast‐derived hormones may contribute to the emerging function of the skeleton as a regulator of energy metabolism.

TL;DR: FoxO1 expressed in osteoblasts is identified as a factor affecting hematopoiesis and a molecular mechanism whereby the FoxO1/activated β-catenin interaction results in AML is provided, which support the notion that the bone marrow niche is an instigator of leukemia and raise the prospect that FoxO 1 oncogenic properties may occur in other tissues.

TL;DR: It is found that the transcription factor FOXO1 is a crucial determinant of the effects of duodenum-derived serotonin on bone formation, and is identified as the molecular node of an intricate transcriptional machinery that confers the signal ofduodenal- derived serotonin to inhibit bone formation.