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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.
Infants with KMT2A-rearranged B-cell acute lymphoblastic leukemia (ALL) have high rates of relapse and poor survival compared with children. Few new therapies have been identified over the past twenty years. The aim of this study was to identify existing anti-cancer agents that have the potential to be repurposed for the treatment of infant ALL.
We identified consistent hypomethylation of the CTGF locus in primary pre-B ALL specimens regardless of CTGF expression.
To identify links between drug resistance and gene deregulation we used oligonucleotide microarray technology.
We hypothesized that reactivation of p53 by inhibition of its negative regulator will result in p53-mediated growth arrest and apoptosis.
Investigation of this rare mixed lineage leukemia cytogenetic abnormality aims to provide further evidence of the genetic changes that underpin this leukemia.
Sébastien Malinge PhD Laboratory Head, Translational Genomics in Leukaemia, Senior Research Fellow (University of Western Australia), Adjunct Senior
Laurence Rishi S. Sébastien Cheung Kotecha Malinge BPharm (Hons) MBA PhD MB ChB (Hons) MRCPCH FRACP PhD PhD Co-Head, Leukaemia Translational Research
B-cell acute lymphoblastic leukaemia (B-ALL) is characterised by diverse genomic alterations, the most frequent being gene fusions detected via transcriptomic analysis (mRNA-seq). Due to its hypervariable nature, gene fusions involving the Immunoglobulin Heavy Chain (IGH) locus can be difficult to detect with standard gene fusion calling algorithms and significant computational resources and analysis times are required. We aimed to optimize a gene fusion calling workflow to achieve best-case sensitivity for IGH gene fusion detection.
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.