https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46767 HIST1H3B/C and H3F3A), altering the epigenetic landscape of primitive oligodendrocyte or astrocyte precursor cells of the pontine region of the brainstem. Lysine‐to‐methionine point mutations at amino acid 27 (H3K27M) co‐occur with alterations in signaling genes, including the receptor tyrosine kinases (PDGFR/KIT/VEGFR/MET/EGFR), activin A receptor (ACVR1), intracellular kinases (PI3K/AKT/mTOR), cyclin‐dependent kinases (CDKs1/4/6), transcriptional regulators (MYCN), and tumor suppressors (PTEN/TP53). This cooperation drives gene expression signatures that inhibit cellular differentiation (ID1/2, Hedgehog) and promotes malignant transformation. Unique to DIPG, is the frequency of co‐occurring sets of genomic insults. However, mapping of the oncogenic signaling pathways activated in response to recurring mutations is unresolved. Herein, known oncogenic signal pathways activated in response to recurring somatic mutations and gene amplifications in DIPG are reviewed. Additionally, an important role for high‐resolution quantitative proteomics/phosphoproteomics in the characterization of signaling cascades are highlighted. These regulate the cell cycle, epigenetics and anti‐apoptotic processes, information critical for the development of improved treatment strategies for DIPG.]]> Wed 30 Nov 2022 11:45:04 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39993 p < 5 x 10⁻⁸) in either cohort. Among the top 34 single-nucleotide polymorphisms (SNPs) (p < 1 x 10⁻⁶), two loci had concordant effects in both cohorts: ALOX15B (rs1804772) (MAF: 1%; p = 3.95 x 10⁻⁷) that influences arachidonic acid metabolism and thus platelet aggregation, and KALRN (rs570684) (MAF: 1%; p = 4.34 x 10⁻⁷) that has been previously associated with risk of ischemic stroke, atherosclerosis, and early-onset coronary artery disease. Conclusion: This represents the largest GWAS meta-analysis conducted to date associating SNPs to VTE in children and adolescents treated on childhood ALL protocols. Validation of these findings is needed and may then lead to patient stratification for VTE preventive interventions. As VTE hemostasis involves multiple pathways, a more powerful GWAS is needed to detect combination of variants associated with VTE.]]> Wed 20 Jul 2022 14:36:48 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14363 + and SAP^-cells. This represents the human equivalent of a mixed bone marrow chimera in mice. While memory CD8⁺ T cells specific for CMV and influenza were distributed across SAP⁺ and SAP^- populations, EBV-specific cells were exclusively SAP⁺. The preferential recruitment of SAP⁺ cells by EBV reflected the tropism of EBV for B cells, and the requirement for SAP expression in CD8⁺ T cells for them to respond to Ag-presentation by B cells, but not other cell types. The inability of SAP^- clones to respond to Ag-presenting B cells was overcome by blocking the SLAM receptors NTB-A and 2B4, while ectopic expression of NTB-A on fibroblasts inhibited cytotoxicity of SAP^- CD8⁺ T cells, thereby demonstrating that SLAM receptors acquire inhibitory function in the absence of SAP. The innovative XLP carrier model allowed us to unravel the mechanisms underlying the unique susceptibility of XLP patients to EBV infection in the absence of a relevant animal model. We found that this reflected the nature of the Ag-presenting cell, rather than EBV itself. Our data also identified a pathological signalling pathway that could be targeted to treat patients with severe EBV infection. This system may allow the study of other human diseases where heterozygous gene expression from random X-chromosome inactivation can be exploited.]]> Wed 11 Apr 2018 13:37:53 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23657 Wed 11 Apr 2018 13:34:30 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41430 Wed 03 Aug 2022 14:12:29 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44354 Tue 11 Oct 2022 19:42:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19876 Tue 09 Jun 2020 09:48:40 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50562 Tue 01 Aug 2023 10:19:27 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55040 Thu 04 Apr 2024 13:51:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15288 Sat 24 Mar 2018 08:21:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12485 Sat 24 Mar 2018 08:15:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12863 40 ng/mL). The majority (> 80%) had plasma levels of vitamins A and E and β-carotene within the normal range. Superoxide dismutase activity was lower than the reference range (< 2.4 U/mg Hb) in all patients, whereas erythrocyte glutathione peroxidase activity was lower than the reference range in 46%. Advanced-stage cancer was associated with increased lipid peroxidation but treatment-related factors or use of dietary supplements was not, suggesting that the oxidant-antioxidant balance may be disturbed in a large proportion of this group. Prospective studies would establish whether antioxidant supplementation plays a role in clinical treatment for pediatric oncology patients.]]> Sat 24 Mar 2018 08:14:48 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:12864 Sat 24 Mar 2018 08:14:47 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26709 Sat 24 Mar 2018 07:26:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27000 50. A Cox multivariate regression model for LFS retained both B-other ALL subtype (hazard ratio 4·1, P = 0·0062) and MRD persistence post-HSCT (hazard ratio 3·9, P = 0·0070) as independent adverse prognostic variables. Persistent MRD could be used to direct post-HSCT therapy.]]> Sat 24 Mar 2018 07:25:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22368 Sat 24 Mar 2018 07:09:30 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48191 Sat 11 Mar 2023 12:30:28 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49579 Mon 22 May 2023 11:19:14 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46401 P < .001). Two-thirds of the post-antibiotic BSIs were associated with a new episode of fever or clinical instability, and only 2 new BSIs were identified after 48 hours of empiric antibiotics and persistent fever. A contaminated BC was identified more frequently in post-antibiotic cultures. Conclusions: In the absence of new fever or clinical instability, BCs beyond 48 hours of persistent fever have limited yield. Opportunity exists to optimize BC collection in this population and reduce the burden of unnecessary tests on patients, healthcare workers, and hospitals.]]> Mon 21 Nov 2022 15:10:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48482 Mon 20 Mar 2023 10:27:49 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48481 Mon 20 Mar 2023 09:59:40 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47905 5 years postdiagnosis. Parents reported on their child's HRQoL (Kidscreen-10), and their own HRQoL (EQ-5D-5L). Parents rated their resilience and fear of cancer recurrence and listed their child's cancer-related late effects. Results: One hundred eighty-two parents of survivors (mean age = 12.4 years old and 9.7 years postdiagnosis) participated. Parent-reported child HRQoL was significantly lower than population norms (48.4 vs. 50.7, p < .009). Parents most commonly reported that their child experienced sadness and loneliness (18.1%). Experiencing more late effects and receiving treatments other than surgery were associated with worse child HRQoL. Parents’ average HRQoL was high (0.90) and no different to population norms. However 38.5% of parents reported HRQoL that was clinically meaningfully different from perfect health, and parents experienced more problems with anxiety/depression (43.4%) than population norms (24.7%, p < .0001). Worse child HRQoL, lower parent resilience, and higher fear of recurrence was associated with worse parent HRQoL. Conclusions: Parents report that young survivors experience small but significant ongoing reductions in HRQoL. While overall mean levels of HRQoL were no different to population norms, a subset of parents reported HRQoL that was clinically meaningfully different from perfect health. Managing young survivors’ late effects and improving parents’ resilience through survivorship may improve HRQoL in long-term survivorship.]]> Mon 06 Feb 2023 15:07:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19772 Fri 29 May 2020 17:14:37 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48462 Fri 17 Mar 2023 12:14:40 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39992 p < 0.001). Many survivors and parents have unmet needs for genetics-related services and information. Greater access to services and information might allow survivors at high risk for late effects to detect and prevent side effects early and improve medical outcomes. Addressing families’ needs and preferences during survivorship may increase satisfaction with survivorship care.]]> Fri 15 Jul 2022 10:13:46 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44512 Fri 14 Oct 2022 09:11:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51529 Fri 08 Sep 2023 12:10:33 AEST ]]>