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Using ClonTracer, a high-complexity genetic barcoding system with the capacity to uniquely label millions of cells with different DNA barcode sequences, Bhang et al. (p 440) show that in preclinical cancer models, the majority of resistant clones already preexist as rare subpopulations prior to therapy and selectively escape therapy. This technology can be used to prioritize combination therapies with distinct resistance mechanisms with the goal of preventing the emergence of resistance. Artwork by Alan Abrams.
Recent clinical data suggest that combination immunotherapy may be the wave of the future. To capitalize on these exciting findings, the scientific, logistical, proprietary and financial hurdles to the clinical testing of combination therapy must be addressed.
A new study reveals that B cells restrict the transendothelial migration of T cells in physiological inflammation in response to adiponectin, but that this mechanism is compromised in autoimmunity and is hence a novel avenue for therapy development.
To target and kill cancer cells, oncolytic viruses exploit signaling pathways that promote tumor growth. A new study shows that the cancer stromal fibroblast factor FGF2 is a crucial component of a tumor–TGF-β axis that renders cancer cells sensitive to virus infection.
The maintenance of blood glucose involves the coordination of multiple organ systems. Two new studies indicate that metformin and resveratrol activate metabolic sensors in the duodenum and initiate a neural loop that reduces liver glucose production in rat models of type 2 diabetes.
Neuropathic pain is a debilitating condition affecting millions of people worldwide. A new study investigates mechanisms of neuropathic pain initiation and identifies a promising therapeutic currently used for acute respiratory distress syndrome that may also limit acute neuropathic pain.
In this Perspective, Fred De Sauvage and Stephen Gould discuss the suitability of different mouse models for modeling cancer pathogenic processes, with an emphasis on applicability to developing cancer therapies.
The authors have developed a barcoded library that enables the high-throughput tracking of tumor cell dynamics and clonal evolution in response to therapy.
All-trans retinoic acid binds to, inhibits and induces degradation of the active form of the prolyl isomerase Pin1, thereby turning off and on a variety of Pin1 substrate oncogenes and tumor suppressors, respectively.
Slit ligand–Robo receptor signaling is needed for developmental angiogenesis in the retina and represents a therapeutic target in ocular neovascular diseases.
An siRNA targeting antithrombin promotes hemostasis in mouse and nonhuman primate models of hemophilia and could represent a new therapeutic option for this disease.
Two papers show that Ampk and Sirt1 respond to metformin and resveratrol, respectively, in the duodenum to initiate a gut-brain-liver axis that reduces hepatic glucose production, thus explaining the antidiabetic actions of these two class of drugs.
Two papers show that Ampk and Sirt1 respond to metformin and resveratrol, respectively, in the duodenum to initiate a gut-brain-liver axis that reduces hepatic glucose production, thus explaining the antidiabetic actions of these two class of drugs.
The recently approved drug dapagliflozin is now shown to increase glucagon secretion by acting on pancreatic alpha cells, which has implications for the potency of its antidiabetic effects
Gianpietro Dotti and colleagues report that CAR-T cells expressing heparanase to degrade the extracellular matrix may enhance their infiltration of and effects on solid tumors.
John Bell and colleagues report that cross-talk between tumor and cancer-associated fibroblasts mediated by FGF2 can enhance efficacy of oncolytic virotherapy.