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A new approach to tumor therapy combines two problematic cancer-fighting tools: tumor-targeted T cells and gene therapy. The T cells deliver a gene therapy vector to tumor cells, ensuring their destruction (pages 1073–1081).
In susceptible individuals, fasting can trigger an attack of acute porphyria—a syndrome caused by the neurotoxic effects of precursors to porphyrins. The mechanistic basis for this trigger is now uncovered.
Liver regeneration can occur by proliferation of two different cell types, but generally only one at a time is fully turned on. A factor that may specifically activate one of these cell types now comes to light.
The hormone adiponectin is secreted from fat cells and increases sensitivity to insulin in muscle and liver; adiponectin increases resistance to metabolic disorders and, it now appears, may also protect heart tissue when blood flow is restricted (pages 1096–1103).
Results now emerge from a preclinical trial of a heat-shock protein inhibitor in a mouse model of neurodegenerative disease. The data indicate that targeting a misfolded protein for degradation may be a useful therapeutic strategy (pages 1088–1095).
Antibiotic discovery has been stalled for well over a decade. The discovery of a new antibiotic with an unexpected mechanism of action could reinvigorate this lagging field (pages 1082–1087).
Normal cells can respond to expression of activated oncogenes by initiating cellular senescence, a permanent state of proliferative arrest. But whether this process reflects a relevant anticancer mechanism has been debated. Several studies now show that oncogene-induced senescence can occur in vivo and provides a bona fide barrier to tumorigenesis.
Neurons in the brain of individuals with focal epilepsy exhibit sustained discharges, called paroxysmal depolarization shifts. Unexpected new evidence indicates that glutamate release from glia can generate these events, and may serve to synchronize the activity of neurons (pages 973–981).
Loss of the transcription factor Gax is at the center of blood vessel dysregulation in the brain and contributes to Alzheimer disease pathology (pages 959–965).
Fresh approaches are needed for antiangiogenesis therapies that target blood vessel growth in tumors. Knocking down multiple regulators of angiogenesis might provide a way forward (pages 992–997).
Plague bacteria are renowned for causing some of the most devastating epidemics in human history. We are now closer to understanding why: the pathogen selectively disarms key cells of the innate immune system, weakening the front-line defenses of the body.
Molecules that recognize pathogens and activate the immune response are being discovered at a rapid rate. RIG-I, a new protein in this category, recognizes viral RNA. Recent studies show that RIG-I operates independently of Toll-like receptors and that it is targeted for inactivation by the hepatitis C virus.
The bacterium that causes Lyme disease is a manipulative creature. This pathogen exploits a component in the saliva of its vector, a tick, to facilitate invasion of vertebrate hosts.
Adult stem cells can self-renew and can give rise to committed progenitors—but definitive evidence of cells with both properties is lacking in most tissues. A cell in skeletal muscle, the satellite cell, now meets these criteria.
