Recognition of transformed cells by the immune system can sometimes generate a rate-limiting equilibrium phase, wherein tumor outgrowth is prevented without complete neoplasm elimination. Targeting premalignancies during this immune-controlled bottleneck is a promising strategy for rational cancer prevention. Thus far, immune equilibrium has been difficult to model in a traceable way, and most immunoediting systems have been limited to mesenchymal tumor types.
View Article and Find Full Text PDFBackground: Nicotinic acetylcholine receptors have gained attention in the last several years as mediators of alcohol-related behaviors. The genes that code for the α5, α3, and β4 subunits (Chrna5, Chrna3, and Chrnb4, respectively) map adjacent to each other on human chromosome 15/mouse chromosome 9. Genetic variants in this region have been associated with alcohol phenotypes and mice that overexpress these three subunits have reduced ethanol intake.
View Article and Find Full Text PDFThe mesolimbic dopaminergic pathway has been implicated in many rewarding behaviors, including the consumption of ethanol and voluntary exercise. It has become apparent that different rewarding stimuli activate this pathway, and therefore it is possible for these behaviors to influence each other, i.e.
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