A MODEL FOR LIFE
Summary: We spoke to Lewis Cantley about his career path and the story behind some of his key breakthroughs, including discovery of the phosphoinositide 3-kinase signaling pathway and insights into the role of dysregulated metabolism in cancer.
Summary: This Review highlights a Drosophila model of diet-induced obesity and cancer, and how these two models are combined to study the interplay between obesity and cancer.
A human pluripotent stem cell model of catecholaminergic polymorphic ventricular tachycardia recapitulates patient-specific drug responses
Editors' choice: Clinically observed drug response differentials to β-blocker and flecainide treatment in catecholaminergic polymorphic ventricular tachycardia can be modeled in vitro using patient-derived iPSC-cardiomyocytes.
The ALK inhibitor PF-06463922 is effective as a single agent in neuroblastoma driven by expression of ALK and MYCN
Summary: Our results suggest that PF-06463922 is a potent inhibitor of crizotinib-resistant ALK mutations, and highlights an important new treatment option for neuroblastoma patients.
Small heat shock proteins mediate cell-autonomous and -nonautonomous protection in a Drosophila model for environmental-stress-induced degeneration
Summary: A Drosophila model for environmental-stress-induced degeneration exhibits key features for genetic analysis of degenerative disease mechanisms and reveals new forms of protection mediated by small heat shock proteins.
Summary: Igf1-deficient mice show chronic inflammation in the retina, and we reveal that controlling inflammation through autophagy in young mice could prevent loss of retinal function.
A knockin mouse model for human ATP4aR703C mutation identified in familial gastric neuroendocrine tumors recapitulates the premalignant condition of the human disease and suggests new therapeutic strategies
Summary: Gastric pathologies in an ATP4a knockin mouse model of a mutation responsible for the development of gastric neuroendocrine tumors in humans are prevented and reverted by adding HCl to drinking water.
A mouse model for ulcerative colitis based on NOD-scid IL2R γnull mice reconstituted with peripheral blood mononuclear cells from affected individuals
Summary: The phenotype and colitis-like symptoms induced in NSG mice reconstituted with PBMCs derived from ulcerative-colitis-affected donors reflect the human disease.
Progressive neurologic and somatic disease in a novel mouse model of human mucopolysaccharidosis type IIIC
Summary: A new animal model of the severe neurodegenerative lysosomal disorder mucopolysaccharidosis IIIC recapitulates the human disease, with progressive CNS and somatic lysosomal pathology, and shortened lifespan.
A mouse model for fucosidosis recapitulates storage pathology and neurological features of the milder form of the human disease
Summary: The fucosidosis mouse model aids understanding of general pathophysiological mechanisms underlying α-L-fucosidase deficiency and is urgently required to establish therapeutic approaches.
A high-fat jelly diet restores bioenergetic balance and extends lifespan in the presence of motor dysfunction and lumbar spinal cord motor neuron loss in TDP-43A315T mutant C57BL6/J mice
Summary: A high-fat diet extends lifespan in a TDP-43 mutant mouse model of motor neuron disease and might be a possible treatment strategy for individuals with amyotrophic lateral sclerosis.
Systematic identification of genes involved in metabolic acid stress resistance in yeast and their potential as cancer targets
Summary: Altered metabolism in tumours creates metabolic acid stress in tumour cells, which is a target for chemotherapeutics. We identify six new complexes with roles in resistance to metabolic acid stress.
Autocrine IL-10 activation of the STAT3 pathway is required for pathological macrophage differentiation in polycystic kidney disease
Summary: Macrophages in polycystic kidney disease are induced by cyst epithelial cell factors to perform pathological pro-proliferative functions through stimulation of an autocrine IL-10–STAT3 pathway.