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Nature Medicine

Nature Medicine is the premier journal for biomedical research. Respected internationally for the quality of its papers on areas ranging from infectious disease to cancer and neurodegeneration, Nature Medicine aims to bridge the gap between basic research and medical advances and is consistently ranked the number one journal by the Institute of Scientific Investigation in the Medicine, Research and Experimental category.
Nature Medicine
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.

By using gene expression data, gastric cancer is divided into subtypes associated with distinct molecular alterations and clinical prognosis.

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.

B cell–mediated inhibition of T cell trafficking is impaired in inflammatory disease.

A photovoltaic retinal prosthesis activated by light restores half of normal visual acuity in rats blinded by retinal degeneration.

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

Inhibition of T cell–derived leukocyte elastase by neuronal SerpinA3N or the drug Sivelestat reduces neuropathic pain.

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.