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Siblings of children with cancer have been shown to experience disruption in multiple domains including family, school, and friendships. Existing literature on siblings' experiences focuses on older children or on a broad range of ages.
The vascular endothelial growth factors and their receptors are key regulators of blood vessel formation, including in tumors, where their deregulated function can promote the production of aberrant, leaky blood vessels, supporting tumor development.
Event-free survival considers other adverse events in addition to mortality. It therefore provides a more complete understanding of the effectiveness and consequences of treatment than standard survival measures, but is rarely reported at the population level for childhood cancer.
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.
Copy 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.
Transcriptional cofactors of the ETO family are recurrent fusion partners in acute leukemia. We characterized the ETO2 regulome by integrating transcriptomic and chromatin binding analyses in human erythroleukemia xenografts and controlled ETO2 depletion models. We demonstrate that beyond its well-established repressive activity, ETO2 directly activates transcription of MYB, among other genes.
Invasive fungal disease (IFD) occurs less frequently during treatment for solid compared to hematological malignancies in children, and risk groups are poorly defined. Retrospective national multicenter cohort data (2004-2013) were analyzed to document prevalence, clinical characteristics, and microbiology of IFD.
BRAF genomic alterations are the most common oncogenic drivers in pediatric low-grade glioma.
Standard-risk WNT medulloblastoma patients have an excellent prognosis using the combination of standard dose craniospinal radiotherapy (CSI) followed by platinum and alkylator based chemotherapy. A recent pilot study that attempted to completely omit radiotherapy was terminated early as all patients relapsed rapidly. The study highlights that therapy is the most important prognostic factor, with CSI still required to cure even the most favorable subgroup of medulloblastoma patients.
RNA-sequencing (RNA-seq) efforts in acute lymphoblastic leukaemia have identified numerous prognostically significant genomic alterations which can guide diagnostic risk stratification and treatment choices when detected early.