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Showing results for "rishi kotecha"
Development of standardised guidance by national and regional authorities for reducing the risk of SARS-CoV-2 transmission to children with cancer
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
Rishi S. Kotecha MB ChB (Hons) MRCPCH FRACP PhD Co-Head, Leukaemia Translational Research rishi.kotecha@health.wa.gov.au Co-Head, Leukaemia
ETV6::RUNX1 is one of the most common recurrent genomic abnormalities in acute lymphoblastic leukaemia (ALL) and is associated with a good prognosis. High expression of NTRK1, encoding tropomyosin receptor kinase A (TrkA), confers a poor prognosis in other malignancies and may contribute to therapy resistance in patients with ETV6::RUNX1 B-ALL.
Parents of children with acute lymphoblastic leukaemia (ALL) experience emotional distress throughout their child's treatment course. This study describes the psychological experience of Australian and New Zealand parents of children diagnosed with ALL.
Acute lymphoblastic leukaemia (ALL) is the most common paediatric malignancy and remains one of the most common causes of cancer-related death in children and adolescents. Five-year overall survival rates now exceed 90% with current multidrug chemotherapeutic regimens.
Children receiving treatment for acute myeloid leukemia (AML) are at high risk of invasive fungal disease (IFD). Evidence from pediatric studies support the efficacy of antifungal prophylaxis in reducing the burden of IFD in children receiving therapy for AML, yet existing antifungal agents have specific limitations and comparative data to inform the optimal prophylactic approach are lacking.
Children with Down syndrome (DS) are at increased risk of developing haematological malignancies, in particular acute megakaryoblastic leukaemia and acute lymphoblastic leukaemia. The microenvironment established by abnormal haematopoiesis driven by trisomy 21 is compounded by additional genetic and epigenetic changes that can drive leukaemogenesis in patients with DS.