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Insights into the Clinical, Biological and Therapeutic Impact of Copy Number Alteration in CancerCopy number alterations (CNAs), resulting from the gain or loss of genetic material from as little as 50 base pairs or as big as entire chromosome(s), have been associated with many congenital diseases, de novo syndromes and cancer. It is established that CNAs disturb the dosage of genomic regions including enhancers/promoters, long non-coding RNA and gene(s) among others, ultimately leading to an altered balance of key cellular functions.
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The bone marrow microenvironment of pre-B acute lymphoblastic leukemia at single-cell resolutionThe bone marrow microenvironment plays a key role in leukemia progression, but its molecular complexity in pre-B cell acute lymphoblastic leukemia (B-ALL), the most common cancer in children, remains poorly understood. To gain further insight, we used single-cell RNA sequencing to characterize the kinetics of the murine BMM during B-ALL progression.
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Lightening the leukaemia load for kids with Down syndromeKids born with Down syndrome are at high risk of an array of health problems. One of the lesser-known complications is their increased risk of childhood leukaemia.
Research
Novel therapeutics approaches for infants with high-risk infant acute lymphoblastic leukaemiaRishi S. Laurence Sébastien Kotecha Cheung Malinge MB ChB (Hons) MRCPCH FRACP PhD BPharm (Hons) MBA PhD PhD Co-Head, Leukaemia Translational Research
Research
Delivery of PEGylated liposomal doxorubicin by bispecific antibodies improves treatment in models of high-risk childhood leukemiaHigh-risk childhood leukemia has a poor prognosis because of treatment failure and toxic side effects of therapy. Drug encapsulation into liposomal nanocarriers has shown clinical success at improving biodistribution and tolerability of chemotherapy. However, enhancements in drug efficacy have been limited because of a lack of selectivity of the liposomal formulations for the cancer cells.
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Biologic and Clinical Analysis of Childhood Gamma Delta T-ALL Identifies LMO2/STAG2 Rearrangements as Extremely High RiskAcute lymphoblastic leukemia expressing the gamma delta T-cell receptor (γδ T-ALL) is a poorly understood disease. We studied 200 children with γδ T-ALL from 13 clinical study groups to understand the clinical and genetic features of this disease. We found age and genetic drivers were significantly associated with outcome.
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Minimising Adverse Drug Reactions and Verifying Economic Legitimacy-Pharmacogenomics Implementation in Children (MARVEL- PIC): protocol for a national randomised controlled trialDNA-informed prescribing (termed pharmacogenomics, PGx) is the epitome of personalised medicine. Despite international guidelines existing, its implementation in paediatric oncology remains sparse.
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Potent antileukemic activity of curaxin CBL0137 against MLL-rearranged leukemiaThe aim of our study was to investigate whether CBL0137 has potential as a therapeutic and chemopotentiating compound in MLL-r leukemia
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Are outcomes for childhood leukaemia in Australia influenced by geographical remoteness and Indigenous race?Presenting features, biology and outcome for childhood leukaemia are known to vary by ethnic origin, geographic location and socioeconomic group. This study aimed to compare presentation patterns, follow-up and clinical outcomes in Indigenous and non-Indigenous children with acute leukaemia in Australia, and to assess the impact of remoteness and area-based socioeconomic disadvantage on outcome.
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Clinical Implications of Minimal Residual Disease Detection in Infants With KMT2A-Rearranged Acute Lymphoblastic Leukemia Treated on the Interfant-06 ProtocolInfant acute lymphoblastic leukemia (ALL) is characterized by a high incidence of KMT2A gene rearrangements and poor outcome. We evaluated the value of minimal residual disease (MRD) in infants with KMT2A-rearranged ALL treated within the Interfant-06 protocol, which compared lymphoid-style consolidation (protocol IB) versus myeloid-style consolidation (araC, daunorubicin, etoposide/mitoxantrone, araC, etoposide).