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Abacavir inhibits but does not cause self-reactivity to HLA-B*57:01-restricted EBV specific T cell receptors

Pre-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.

Diverse Anti-Tumor Immune Potential Driven by Individual IFNα Subtypes

Our data shows that the expression of distinct IFNα subtypes within the tumor microenvironment results in different anti-tumor activities

MK2 inhibition induces p53-dependent senescence in glioblastoma cells

In response to DNA damaging chemotherapy, targeting MK2 in p53-mutated cells produces a phenotype that is distinct from the p53-deficient phenotype

Simultaneous Targeting of DNA Replication and Homologous Recombination in Glioblastoma with a Polyether Ionophore

Our findings highlight the potential of salinomycin to induce DNA lesions and inhibit homologous recombination to greatly enhance the effect of radiotherapy

Understanding acute burn injury as a chronic disease

The review will outline evidence of long-term health effects, possible mechanisms linking burn injury to long-term health and current research into burns as a chronic disease

Most clinical anti-EGFR antibodies do not neutralize both wtEGFR and EGFRvIII activation in glioma

We discovered a previously unknown major resistance mechanism in glioma in that most EGFR domain III-targeting antibodies do not neutralize EGFRvIII

A reference collection of patient-derived cell line and xenograft models of proneural, classical and mesenchymal glioblastoma

We present a curated panel of 12 readily-usable, cell lines representing the spectrum of molecular subtypes of IDH-wildtype glioblastoma

PI3K activation in neural stem cells drives tumorigenesis which can be ameliorated by targeting the cAMP response element binding protein

A novel mouse model for glioma demonstrating that the PI3K pathway is important for initiation of tumorigenesis

Activation of ERBB4 in Glioblastoma Can Contribute to Increased Tumorigenicity and Influence Therapeutic Response

Despite low ERBB4 mRNA in glioblastoma, the functional effects of increased ERBB4 activation identify ERBB4 as a potential prognostic and therapeutic target

Activation of ERBB4 in Glioblastoma Can Contribute to Increased Tumorigenicity and Influence Therapeutic Response

The functional effects of increased ERBB4 activation identify ERBB4 as a potential prognostic and therapeutic target