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Immune checkpoint therapy responders display early clonal expansion of tumor infiltrating lymphocytesImmune checkpoint therapy (ICT) causes durable tumour responses in a subgroup of patients, but it is not well known how T cell receptor beta (TCRβ) repertoire dynamics contribute to the therapeutic response.
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Celebrating 100 years of Immunology & Cell Biology – a special focus on the field of tumor immunology in AustraliaIn this Commentary article, as part of the 100-year celebrations of the journal, we reflect on the contribution of articles published in ICB in the field of tumor immunology. A highlight is a series of interviews conducted with three Australian-based ICB authors who have contributed key papers over the years: Rajiv Khanna, Delia Nelson and Ian Frazer.
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Catalysing change in health and medical research policy: an Australian case study of deliberative democracy to reform sex and gender policy recommendationsRevising public health policy based on new data does not happen automatically. This is acutely relevant to the now undeniable evidence that many diseases develop differently between the sexes and may also be affected by gender. Current health and medical practices across the globe generally fail to cater for sex and gender effects in common diseases.
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Transcriptional rewiring in CD8+ T cells: implications for CAR-T cell therapy against solid tumoursT cells engineered to express chimeric-antigen receptors (CAR-T cells) can effectively control relapsed and refractory haematological malignancies in the clinic. However, the successes of CAR-T cell therapy have not been recapitulated in solid tumours due to a range of barriers such as immunosuppression, poor infiltration, and tumour heterogeneity.
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Kids are not small adults, Identifying age-dependent drug targets in paediatric oncologyCancers in children are very different to cancers in adults. However, most therapeutic strategies are designed explicitly for adult cancers, and then used in children if proven safe.
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The interplay between sarcoma and surgery-induced wound healingIn this project, we are using systems biology approaches to map the wound healing response in sarcoma following surgery to identify new treatments that can prevent sarcoma relapse.
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Simultaneous Targeting of DNA Replication and Homologous Recombination in Glioblastoma with a Polyether IonophoreOur findings highlight the potential of salinomycin to induce DNA lesions and inhibit homologous recombination to greatly enhance the effect of radiotherapy
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Retinoic Acid Induces an IFN-Driven Inflammatory Tumour Microenvironment, Sensitizing to Immune Checkpoint TherapyWith immune checkpoint therapy (ICT) having reshaped the treatment of many cancers, the next frontier is to identify and develop novel combination therapies to improve efficacy. Previously, we and others identified beneficial immunological effects of the vitamin A derivative tretinoin on anti-tumour immunity.
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Comprehensive Testing of Chemotherapy and Immune Checkpoint Blockade in Preclinical Cancer Models Identifies Additive CombinationsAntibodies that target immune checkpoints such as cytotoxic T lymphocyte antigen 4 (CTLA‐4) and the programmed cell death protein 1/ligand 1 (PD-1/PD-L1) are now a treatment option for multiple cancer types. However, as a monotherapy, objective responses only occur in a minority of patients. Chemotherapy is widely used in combination with immune checkpoint blockade (ICB). Although a variety of isolated immunostimulatory effects have been reported for several classes of chemotherapeutics, it is unclear which chemotherapeutics provide the most benefit when combined with ICB.
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Abacavir inhibits but does not cause self-reactivity to HLA-B*57:01-restricted EBV specific T cell receptorsPre-existing pathogen-specific memory T cell responses can contribute to multiple adverse outcomes including autoimmunity and drug hypersensitivity. How the specificity of the T cell receptor (TCR) is subverted or seconded in many of these diseases remains unclear. Here, we apply abacavir hypersensitivity (AHS) as a model to address this question because the disease is linked to memory T cell responses and the HLA risk allele, HLA-B*57:01, and the initiating insult, abacavir, are known.