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Acquired resistance during adoptive cell therapy by transcriptional silencing of immunogenic antigensThese findings suggest that tumor cells employ multiple epigenetic and genetic mechanisms to evade immune control
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Risk factors for symptomatic venous thromboembolism during therapy for childhood acute lymphoblastic leukemiaWe found two known risk factors in a large cohort of children treated for ALL and identified other factors associated with venous thromboembolism
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Cochrane corner: platinum-induced hearing loss after treatment for childhood cancerThis systematic review shows that children treated with platinum analogues are at risk of developing hearing loss
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Dendritic cells and cancer: From biology to therapeutic interventionIn this review, we discuss the different subsets of tumor-infiltrating dendritic cells and their role in anti-tumor immunity
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The Australian and New Zealand Children's Haematology/Oncology Group Biobanking NetworkThe ANZCHOG-BN is a new biobank network in Australasia that was developed to improve and streamline access to high-quality pediatric and AYA cancer biospecimens
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Targeting the bone marrow microenvironment: a novel therapeutic strategy for pre-B acute lymphoblastic leukemiaOur findings shed light on the mechanisms of leukemia-induced bone loss
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CD8+XCR1neg Dendritic Cells Express High Levels of Toll-Like Receptor 5 and a Unique Complement of Endocytic ReceptorsOur data demonstrate that CD8+XCR1neg DCs possess a unique pattern of endocytic receptors and a restricted TLR profile that is particularly enriched for TLR5
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Tissue-resident memory CD8+ T cells promote melanoma–immune equilibrium in skinOur results show that TRM cells have a fundamental role in the surveillance of subclinical melanomas in the skin by maintaining cancer-immune equilibrium
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PI3K activation in neural stem cells drives tumorigenesis which can be ameliorated by targeting the cAMP response element binding proteinOur findings present a novel mouse model for glioma demonstrating that the PI3K pathway is important for initiation of tumorigenesis
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Partial trisomy 21 contributes to T-cell malignancies induced by JAK3-activating mutations in murine modelsThis JAK3A572V knockin model is a relevant new tool for testing the efficacy of JAK inhibitors in JAK3-related hematopoietic malignancies