The Vilcek Foundation congratulates the recipients of the 2017 Vilcek Prizes in Biomedical Science.
Lily & Yuh-Nung Jan (University of California, San Francisco) receive $100,000 Vilcek Prize. Michaela Gack (University of Chicago), Michael Halassa (NYU School of Medicine), and Ahmet Yildiz (University of California, Berkeley) each win $50,000 Vilcek Prize for Creative Promise in Biomedical Science.
Nature Milestones: Antibodies chronicles the history of antibodies from their earliest description in antisera, their structure, generation and function, right through to their recent application in cancer immunotherapy. It also includes a timeline and a collection of seminal papers reproduced from Springer Nature.
Take science off the stand p265 doi:10.1038/nm.4303 The scientific process relies on people's willingness to publish data-driven findings. Turning to the legal system to adjudicate the merit of evidence-based assertions in the scientific literature leads us down a dangerous path.
Opioids: keeping the good, eliminating the bad pp272 - 273 Stephanie Puig and Howard B Gutstein doi:10.1038/nm.4277 Two new studies show that mechanisms mediating the opioid side effects of tolerance, hyperalgesia and physical dependence are mediated spinally and can be dissociated from analgesia. These side effects can be selectively targeted by clinically available drugs without affecting their pain-relieving effects.
The shape of the microbiome in early life pp274 - 275 Erika von Mutius doi:10.1038/nm.4299 A recent study shows that microbial-community structure and function substantially expand and diversify in all body sites from birth to age 4-6 weeks. It then resembles microbiota from its corresponding maternal body site, independently of the infant's mode of delivery or other prenatal factors.
Taking inventory of metastasis effectors pp275 - 276 Laura Pisarsky, Jinxiang Dai and Cyrus M Ghajar doi:10.1038/nm.4301 In a recent study in mice, researchers combined tumor barcoding with unbiased genomic analysis and identified Cd109 as a hub gene involved in metastatic progression. They show that pharmacological inhibition of its downstream effectors JAK1 and STAT3 curtails metastatic growth.
α5 nicotinic receptors link smoking to schizophrenia pp277 - 278 Xin-an Liu and Paul J Kenny doi:10.1038/nm.4300 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.
Nature Neuroscience presents this animation, which introduces the molecular, cellular and physiological mechanisms associated with Alzheimer's disease and highlights some of the most recent advances in our understanding of the onset and progression of this devastating neurological condition.
Molecular definition of a metastatic lung cancer state reveals a targetable CD109-Janus kinase-Stat axis pp291 - 300 Chen-Hua Chuang, Peyton G Greenside, Zoe N Rogers, Jennifer J Brady, Dian Yang et al. doi:10.1038/nm.4285 In vivo screening of pro-metastatic factors in a genetically engineered mouse model of lung cancer uncovered the CD109-JAK-STAT3 axis as a key contributor of metastatic dissemination of lung cancer cells. Activation of this pathway predicts poor outcome in patients with cancer, and its pharmacological inhibition dramatically reduces the metastatic ability of tumor cells, suggesting that it might be an effective intervention in patients.
Nicotine reverses hypofrontality in animal models of addiction and schizophrenia pp347 - 354 Fani Koukouli, Marie Rooy, Dimitrios Tziotis, Kurt A Sailor, Heidi C O'Neill et al. doi:10.1038/nm.4274 In transgenic mouse models of neuropsychiatric disease, loss of nicotinic cholinergic signaling in cortical inhibitory interneurons causes neurocognitive behavioral deficits and reduced neuronal activity in prefrontal circuits. Chronic administration of nicotine can restore this cortical hypofrontality phenotype.
Blocking microglial pannexin-1 channels alleviates morphine withdrawal in rodents pp355 - 360 Nicole E Burma, Robert P Bonin, Heather Leduc-Pessah, Corey Baimel, Zoe F Cairncross et al. doi:10.1038/nm.4281 The release of ATP from spinal microglia via pannexin-1 channels is required for withdrawal symptoms after termination of chronic opioid treatment in rodents, and pharmacological blockade of pannexin-1 channels reduces the severity of withdrawal without affecting opiate analgesia.
A distinct innate lymphoid cell population regulates tumor-associated T cells pp368 - 375 Sarah Q Crome, Linh T Nguyen, Sandra Lopez-Verges, S Y Cindy Yang, Bernard Martin et al. doi:10.1038/nm.4278 A previously uncharacterized population of innate lymphoid cells (ILCs) in the tumor microenvironment limits T cell expansion and cytokine production, and associates with early recurrence in patients with cancer. Depletion of this regulatory immunosuppressive cell population overcomes this effect, suggesting important implications for cancer immunotherapy.
DNA methylation heterogeneity defines a disease spectrum in Ewing sarcoma pp386 - 395 Nathan C Sheffield, Gaelle Pierron, Johanna Klughammer, Paul Datlinger, Andreas Schonegger et al. doi:10.1038/nm.4273 DNA methylation sequencing and bioinformatic analyses uncover an epigenetic disease spectrum in Ewing sarcoma. These characteristic epigenome patterns correlate with state of differentiation and disease aggressiveness, and pave the way for the development of biomarkers.
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