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A new study that uses a triple-drug combination to overcome a major mechanism of drug resistance in cancer provides insights into the evolutionary paths taken by tumors in the face of selective pressure.
Using interleukin (IL)-9-deficient mice, Rauber and colleagues unveil a crucial role for group 2 innate lymphoid cells (ILC2s) in the resolution phase of arthritic inflammation, opening up new therapeutic avenues for chronic inflammatory disease.
In this Review, David Fidock discusses malarial resistance to artemisinin-based combination therapies, among others, and presents strategies for designing new therapeutics and to overcome resistance.
A mouse model with combined renal epithelium-specific deletion of Vhl, Trp53 and Rb1 that develops clear-cell renal cell carcinoma provides a research tool for investigating the mechanisms that drive this cancer, and for evaluating the efficacy of novel therapeutic agents.
Enhanced conversion of dietary cholesterol to bile acids through the alternative pathway leads to cold-associated, metabolically beneficial changes in the intestinal microbiome and to elevated bile acid levels that contribute to adaptive thermogenesis.
In this Perspective, Michael Czech presents evidence for whether hyperinsulinemia occurs before insulin resistance upon overfeeding or high-fat diet feeding, or whether insulin resistance causes hyperinsulinemia, thus attempting to delineate the relationship between hyperinsulinemia, obesity and insulin resistance.
New evidence in mouse models reveals that exposure to Δ9-tetrahydrocannabinol (THC), the main psychoactive component in Cannabis sativa, might improve cognitive performance in aging animals.
A recent study has found that rhinovirus-induced exacerbation of asthma is in part mediated by the release of neutrophil extracellular traps and double-stranded DNA by neutrophils in the airway.
A new study reveals that virus-associated activation of a subset of circulating monocytes results in the release of the proinflammatory cytokine tumor necrosis factor (TNF)-α, which induces increased turnover of synapses in the brain and learning deficits in mice.
A new study that uses an integrated single-cell transcriptomics approach to characterize cancer stem cell populations during treatment with molecularly targeted therapies offers insights into disease evolution and points to new therapeutic targets.
Rubin and colleagues discuss the origin and evolution of poorly differentiated neuroendocrine tumors, and highlight potential new therapeutic strategies.
A new study identifies oncostatin M (OSM) as a potential biomarker and therapeutic target for anti-tumor necrosis factor (TNF)-refractory inflammatory bowel disease (IBD), and pinpoints mucosal stromal cells as key players in OSM-mediated inflammation.
A recent study using a humanized mouse model shows that HIV-1 can persist in macrophages during antiretroviral therapy (ART), and suggests that macrophages may represent an obstacle to efforts to cure HIV-1 infection.
A new study in mice suggests that a single drug, thymosin α1, may simultaneously rectify the impaired trafficking of the cystic fibrosis transmembrane conductance regulator (CFTR) in cystic fibrosis (CF) and reduce inflammation, offering new hope for CF treatment.
In this Perspective, June, Bluestone and Warshauer discuss potential cellular and molecular explanations for the autoimmunity often associated with immunotherapy, and propose additional research and changes to reporting practices to aid efforts to understand and minimize these toxic side effects.
A recent study shows that a self-peptide generated in pancreatic islet beta cells through the translation of a noncanonical alternative reading frame in human insulin mRNA is recognized by both CD4+ and CD8+ T cells in type 1 diabetes.
New studies advance the mechanistic understanding of mutant histone H3 in diffuse intrinsic pontine glioma (DIPG) and demonstrate two epigenetic approaches, BET inhibition and EZH2 inhibition, as potential therapeutic strategies for DIPG.
In a recent study, researchers generated a mouse model expressing variant APOL1 that recapitulates human kidney disease. Variant APOL1 leads to caspase-1-dependent pyroptosis, which opens the door for the development of new druggable targets to treat APOL1-mediated kidney disease.
In this Review, Cathomen and colleagues present the latest advances, including improvements in nuclease specificity and delivery, that will expedite the clinical translation of genome editing.
A new study shows that nicotinic receptors activate a particular type of interneuron in the prefrontal cortex. Deficits in this relationship give rise to behavioral abnormalities similar to those associated with schizophrenia, which can be ameliorated by nicotine.
