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Showing results for "rishi kotecha"
We have revealed a novel SH2D1A gene mutation in a patient with XLP resulting in fulminant refractory EBV-driven HLH, which is a recognized severe complication
Our findings shed light on the mechanisms of leukemia-induced bone loss
We report a term male with congenital acute erythroleukemia who achieved sustained remission with low-dose cytosine arabinoside alone
Dr Rishi Kotecha knows too well the devastation of a leukaemia diagnosis in a child, treating children as a consultant at Princess Margaret Hospital.
Four The Kids Research Institute Australia researchers are among those who have received funding in the WA State Government's Merit Award Program announced today.
Osteoclasts are important regulators of bone remodeling, with an established role in maintaining skeletal homeostasis. The emergence of osteoimmunology has identified osteoclasts as key players in the immune system. In particular, osteoclasts can initiate bi-directional crosstalk mechanisms with hematopoietic stem cells and various immune cells, such as T cells, B cells and NK cells, to influence hematopoiesis and inflammatory response.
Invasive fungal disease is a common and important complication in children with acute myeloid leukaemia (AML). We describe the epidemiology of IFD in a large multicentre cohort of children with AML.
Invasive fungal disease (IFD) remains a challenging complication of treatment for paediatric acute leukaemia. Consensus fungal treatment guidelines recommend withholding chemotherapy to facilitate immune recovery in this setting, yet prolonged delays in leukaemia therapy increase risk of relapse.
Invasive fungal disease (IFD) is a common and important complication in children with acute myeloid leukaemia (AML). We describe the epidemiology of IFD in a large multicentre cohort of children with AML.
Components of the bone marrow microenvironment (BMM) have been shown to mediate the way in which leukemia develops, progresses and responds to treatment. Increasing evidence shows that leukemic cells hijack the BMM, altering its functioning and establishing leukemia-supportive interactions with stromal and immune cells.