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The chromatin remodeling complex SWI-SNF is altered in cancer. New findings now show that the core component SNF5 can block a Hedgehog (Hh) effector, which promotes malignant rhabdoid tumor growth when SNF5 is lost (pages 1429–1433). Targeting this Hh effector may be a way to combat these aggressive childhood tumors.
The interaction between two proteins associated with a glutamate receptor can drive neuronal death mediated through this receptor after stroke. A small molecule, designed to specifically disrupt this deadly interaction, protects the brain in mice and rats against neuronal damage without undesirable side effects (pages 1439–1443).
Postoperative ileus complicates the recovery from intestinal surgery with a great economic burden. How this morbid condition spreads throughout the entire gut remains unknown, but new findings show that a T helper type 1 (TH1)-mediated immune response is involved. Its components may be possible therapeutic targets (pages 1407–1413).
Mesenchymal stem cells (MSCs) can form different cell types in culture, but their potential to build new tissue in various disorders where tissue is damaged has not been realized. A study now shows how mature cells from blood vessels are a new source of MSCs that may be used to regenerate cartilage and bone (pages 1400–1406).
A new study in mice and human tissue shows that activation of bitter taste receptors in the airways relaxes airway smooth muscle, resulting in bronchodilation (pages 1299–1304). Agonists of these receptors seem to be better than current β2-adrenergic bronchodilators in a mouse asthma model, suggesting a new way to ease breathing during asthma.
Skeletal muscles in a mouse model of human muscular dystrophy degenerate because of excessive cell death. A new study suggests that these muscles suffer from lack of autophagy, exacerbating apoptosis and mitochondrial dysfunction (pages 1313–1320). Reactivation of autophagy with a low-protein diet may ameliorate muscle myopathy.
Overexpression of T cell leukemia homeobox 1 (TLX1) occurs in some leukemias. New findings in mice and humans show how TLX1 drives chromosomal aberrations and deletions of tumor suppressor genes during T-cell transformation (pages 1321–1327). Surprisingly, its expression does not correlate with bad prognosis.
Depression ruins the lives of millions of people, causing dysphoria and anguish. New findings in rodents and human brain shed light on the mechanisms of this disease, uncovering a phosphatase as a new target to treat depressive behaviors (pages 1328–1332).
Uncovering how the immune system of the mucosa surmounts allergic reactions may open new avenues to treat inflammatory conditions in the gut. New findings in mice now show that a C-type lectin receptor in dendritic cells (DCs) protects against food antigens that cause systemic anaphylaxis—promoting oral tolerance (pages 1128–1133).
Bacterial pneumonia can be a life-threatening disease that causes lung injury. A new study shows that accumulation of a phospholipid in the lung fluid in mice and humans worsens gas exchange during the microbial infection (pages 1120–1127). Clearance of this lipid may improve lung function during infection.
Mobilization of hematopoietic stem cells (HSCs) from the bone marrow is the standard method to collect grafts for stem cell transplants, but sometimes insufficient HSCs are mobilized. A new study suggests that epidermal growth factor receptor (EGFR) inhibition can augment mobilization, bringing us one step closer to an universal method to obtain HSCs for transplantation (pages 1141–1146).
The tumor suppressor p53 is inactivated by genetic mutations in many cancers, except for neuroblastoma. New findings show that this cancer reversibly inhibits p53 through a microRNA, miR-380-5p (pages 1134–1140). Blocking it to restore p53 function may be an attractive therapeutic option for neuroblastomas.
Just as a Bob Marley tune can elicit a visceral pull, a rhythmic awakening can shake up metabolism, with a new study in mice showing that cryptochrome (CRY) in the liver controls glucose levels during fasting and improves insulin sensitivity—introducing a new possible therapy for type II diabetes (pages 1152–1156).
Recent studies show that Musashi-2 (MSI2), a molecule that binds RNA, increases proliferation of normal and malignant blood stem cells. In humans, increased amounts of MSI2 correlate with poor prognosis of leukemia—indicating that MSI2 may be a target to treat this type of cancer.
Thyroid hormones increase the energy metabolism of the body in a process called 'thyroid thermogenesis'. Its molecular mechanism, however, has been elusive. Recent findings in rats suggest that it is localized to brown adipose tissue—our one truly thermogenic organ—and is mediated via the brain (pages 1001–1008).
Thick, adherent mucus in the airway causes respiratory failure—the leading cause of death in cystic fibrosis. A new study now shows how the formation of neutrophil extracellular traps (NETs) in the airway, in an attempt to kill colonizing bacteria, results in chronic cell carnage that thickens the sputum, worsening lung function in individuals with cystic fibrosis (pages 1018–1023).
A drug that discourages alcohol ingestion has shown promise as a treatment for cocaine addiction. New findings in rats suggest a potential mechanism—the drug decreases amounts of dopamine in the brain (pages 1024–1028). Blocking enzymes that regulate dopamine abundance may be a new way to treat cocaine addiction and prevent relapse in humans.
Vaccines can prevent infections by several pathogens. Success, however, has been limited for other chronic diseases, reflecting a constraint for effectively manipulating the human immune system. The results from four studies describe a novel dendritic cell (DC) subset in humans that may be crucial for the design of vaccines against cancer and other chronic diseases.
Elevated amounts of glutamate, which acts as a neurotransmitter but is also a neurotoxin, are a hallmark of the autoimmune neurological disease multiple sclerosis and may contribute to its pathology. The discovery that a receptor for glutamate can inhibit the development of autoimmunity and protect from neuroinflammation in a mouse model of multiple sclerosis suggests that glutamate may also have a protective role and that its receptor may represent a therapeutic target (pages 897–902).
Cancers can compromise the capacity of the host immune system to recognize tumor antigens. Recent findings now show that increased accumulation of lipids in dendritic cells in tumors can impair presentation of tumor antigens—which is crucial for activation of the immune system—providing a conceptual framework that may help increase the efficacy of therapeutic vaccines (pages 880–886).
