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Nature Medicine

A biomedical research journal devoted to publishing the latest and most exciting advances in biomedical research for scientists and physicians.


Calculated risk: a new single-nucleotide polymorphism linked to severe influenza disease


Clear links between human genes and susceptibility to influenza disease are scarce. A recent study uncovers a gene variant coupled to severe influenza, and shows how it hampers the expression of an antiviral gene that is key to immune cell survival.

A three-drug combination to treat BRAF-mutant cancers


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.

Resolving a chronic inflammation mystery


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.

Antimalarial drug resistance: linking Plasmodium falciparum parasite biology to the clinic


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.

An approach to suppress the evolution of resistance in BRAFV600E-mutant cancer


Resistance to ERK signaling inhibitors in BRAFV600E-mutant melanomas and lung cancers is achieved by parallel convergent mechanisms, including amplification of the mutant allele in extrachromosomal elements, that allow tumors to adapt while maintaining their intratumor heterogeneity. Intermittent treatment with a combination of RAF, MEK and ERK inhibitors imposes a higher selective pressure than sequential therapy and produces the strongest antitumor effects while minimizing toxicity. These findings warrant evaluating the effectiveness of this combinatorial regimen in patients, to improve treatment responses and delay the emergence of drug resistance.

Resolution of inflammation by interleukin-9-producing type 2 innate lymphoid cells


Number of IL-9-expressing ILC2s are elevated in patients with inflammatory arthritis during remission, and these cells are critical in mice for the resolution of inflammatory arthritis via regulatory T cell induction. Delivery of DNA minicircles encoding IL-9 into inflamed joints ameliorates mouse experimental arthritis, suggesting possible therapeutic applications.

A tripartite complex of suPAR, APOL1 risk variants and αvβ3 integrin on podocytes mediates chronic kidney disease


A complex of suPAR and high-risk variants of APOL1 acting on integrin signaling in the kidney contributes to APOL1-associated chronic kidney disease.

Reconstruction of the mouse extrahepatic biliary tree using primary human extrahepatic cholangiocyte organoids


Repair of defects in the common bile duct is hampered by a lack of healthy donor tissue. Developing human extrahepatic cholangiocyte organoids and testing them in mouse models may provide a way to overcome this limitation.

Plk1 regulates contraction of postmitotic smooth muscle cells and is required for vascular homeostasis


The kinase Plk1 has been studied primarily as a mitotic regulator in dividing cells, but de Cárcer et al. find that Plk1 deficiency or inhibition in mice causes nonmitotic defects in the vasculature, including aortic aneurysm and rupture, as well as defective vascular smooth muscle contractility. These results recommend a note of caution in the clinical use of PLK1 inhibitors as anticancer agents.

SNP-mediated disruption of CTCF binding at the IFITM3 promoter is associated with risk of severe influenza in humans


IFITM3 encodes an antiviral protein that blocks entry of influenza A virus into cells. Paul Thomas and colleagues report that SNP rs34481144 in the 5′ UTR of IFITM3 is an expression quantitative trait locus for this gene and that the risk allele is associated with lower IFITM3 expression and severe influenza disease.

Correction of a splicing defect in a mouse model of congenital muscular dystrophy type 1A using a homology-directed-repair-independent mechanism


An HDR-independent therapeutic genome-editing approach corrected the splice-site mutation in Lama2 in a mouse model of congenital muscular dystrophy type 1A, and may be applied more broadly to correct splice-site mutations associated with other diseases.

Fibroblast growth factor 19 regulates skeletal muscle mass and ameliorates muscle wasting in mice


FGF19 acts directly on skeletal muscle to increase its mass, and treatment with the hormone ameliorates muscle atrophy in three mouse models.

Inflammation-dependent cerebrospinal fluid hypersecretion by the choroid plexus epithelium in posthemorrhagic hydrocephalus


In a rat model of hydrocephalus triggered by intraventricular hemorrhage, Kristopher Kahle and colleagues show that TLR4–NF-κB-dependent inflammatory signaling in the choroid plexus causes hypersecretion of cerebrospinal fluid that drives hydrocephalus. Targeting TLR4–NF-κB-mediated signaling or the NKCC1–SPAK complex ameliorates hydrocephalus.