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Loss of sympathetic nerve innervention of the bone marrow contributes to the aging of hematopoietic stem cells, which can be rejuvenated using an adrenergic receptor agonist.
Treatment with setmelanotide, a new-generation MC4R agonist, provides durable weight loss in hyperphagic, leptin receptor–deficient patients, suggesting a pharmacological avenue to treat patients with various MC4R pathway defects.
The phase 3 TNT Trial in subjects with triple-negative breast cancer supports the superiority of carboplatin over docetaxel in BRCA1/2-mutated tumors and a greater response to taxanes in the nonbasal subtype.
An IL-6/STAT3 signature and memory CD8 T cell subset in preinfusion chimeric antigen receptor–expressing T cells associate with response in patients with high-risk chronic lymphocytic leukemia.
Comprehensive integration of mutational and structural alterations in clinically-annotated DLBCL patient samples provides a novel molecular classification of the disease.
A shared gene expression program associated with silencing HIV-1 transcription may be critical for persistence of reactivated latent CD4+ T cells in patients with HIV.
The tumor immune microenvironment influences tumor progression and response to immunotherapy; its further characterization will improve therapeutic outcome.
Promoting more bone growth is of keen interest in the treatment of osteoporosis, and preventing the degradation of S1P offers a new therapeutic avenue for this approach.
Keratinocytes require glucose for injury- or inflammation-driven but not homeostatic proliferation, and glucose-transport blockade blocks psoriasis-like pathology in experimental models.
Lethal pediatric tumors bearing a particular histone H3 mutation upregulate the disialoganglioside GD2, thereby making these tumors susceptible to chimeric antigen receptor T cell–based immunotherapy.
In mouse models of stress-induced depression, molecular and chemogenetic stimulation of the entorhinal cortex induces the production of adult-born hippocampal neurons and generates antidepressive-like effects.
Human iPSC-derived neurons are generated from individuals with or without Alzheimer's disease carrying different APOE alleles and reveal a toxic, neuron-intrinsic gain of function of the ApoE4 variant that is a strong genetic risk factor for AD.