Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Using a device implanted in KRAS-driven pancreatic tumors, authors demonstrate that cancer cells incorporate proteins in their microenvironment as a source of amino acids. This work provides a novel approach to study tumor metabolism that could be applied with therapeutic purposes.
A pharmacological screen has identified the histone methyltransferase G9a as a target to reactivate imprinted genes in a mouse model of Prader–Willi Syndrome that improves growth and survival.
Genetic deletion of HDAC3, a circadian epigenome regulator, specifically in skeletal muscle alters amino acid metabolism, leading to increased muscle endurance but at the cost of whole-body insulin resistance.
New vaccine approaches that safely elicit immunity are needed to protect against infectious disease. Erasmus et al. report their development of an insect-virus-based platform that they use to engineer a protective vaccine against chikungunya fever.
The therapeutic response of acute myeloid leukemia to the nucleoside analog Ara-C is controlled by SAMHD1, an enzyme that hydrolyzes the active metabolite Ara-CTP.
Soluble uPAR is known to contribute to certain types of chronic kidney disease, and myeloid cells from the bone marrow have now been shown to be a key source of this factor.
In leukemic mice, fasting reduces the development of acute lymphoblastic leukemia, but not acute myeloid leukemia, via upregulation of leptin receptor expression and signaling in the leukemic cells.
Proteasomal degradation of EZH2 in AML patients in response to therapy triggers the expression of stem cell markers and has been identified as an epigenetic pathway leading to acquired drug resistance. Treatments aimed to restore EZH2 expression in relapsed AML patients have shown clinical efficacy and constitute a viable approach to re-sensitize tumors to chemotherapy.
B cells protect against inflammation-associated preterm labor via IL-33-induced PIBF1 expression in mice, which suggests a therapy for this condition in humans.
Using functional MRI in a large multisite sample of more that 1,000 patients, four distinct neurophysiological biotypes of depression are defined. These biotypes are used to develop diagnostic classifiers that distinguish patients with depression from controls in separate multisite validation and replication cohorts, and can predict patient responsiveness to therapy.
The Wnt pathway inhibitor Dkk1, which is produced by bone marrow osteolineage cells, promotes hematopoietic recovery after radiation injury by both direct effects on hematopoietic cells and indirect effects on bone marrow endothelial cells.
Akkermansia muciniphila, a member of the gut microbiome, has been shown to improve metabolism in mice. Here it is reported that its pasteurization further improves this effect, and that one of its membrane proteins by itself has a similar benefit.
The thalamus-enriched microRNA miR-338-3p is depleted in mouse models of 22q11.2 deletion syndrome and in humans with schizophrenia, leading to a late-onset dysfunction of auditory thalamocortical synaptic transmission, behavioral abnormalities and altered sensitivity to antipsychotics.
By reducing the availability of extracellular L-cyst(e)ine, an engineered enzyme inhibits glutathione production and cripples antioxidant defenses of tumors in a variety of mouse models.
A genome-wide CRISPR screen reveals that FZD5, but none of the other nine Frizzled receptors encoded in the human genome, is a therapeutic vulnerability of pancreatic and colorectal tumors bearing RNF43 mutations.
Organoids formed by combining pluripotent-stem-cell-derived human neural crest cells with pluripotent-stem-cell-derived intestinal tissue show functional interstitial cells of Cajal and undergo waves of contraction; these tissues reveal insights into the molecular defects characterizing Hirschsprung's disease.
Copy-number alterations detected in circulating tumor cells at time of diagnosis predict chemosensitive versus chemorefractory responses; however, CTCs obtained after subsequent relapse bear a chemosensitive copy-number alteration profile, which suggests that different mechanisms drive initial and acquired chemoresistance.
Ram Savan and colleagues report that two miRNAs known to suppress type 3 interferon (IFN) signaling also downregulate type 1IFN signaling in hepatitis C virus (HCV)-infected hepatocytes. The findings provide insights into the mechanisms by which antiviral IFN signaling is inhibited in HCV infection.
Blockade of cIAP1 and cIAP2 induces a tumor cell-autonomous type-I IFN response that activates myeloid cells and potentiates anti-tumor immunity in pre-clinical models and patients with multiple myeloma.
AML cells carrying R882 mutations in DNMT3A fail to sense and repair DNA damage induced by standard-dose chemotherapy as a result of impaired chromatin remodeling