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Hundreds of susceptibility loci have previously been associated with autism spectrum disorder (ASD) suggesting the disease is genetically heterogeneous. In this issue, Stephen Scherer and colleagues report a whole-genome sequencing study of 85 quartet families (parents and two ASD-affected siblings). The cover image, courtesy of Linden Gledhill and Autism Speaks, depicts the growing face of a liquid crystal formed from an evaporating aqueous solution of DNA (specifically, the 14 base pair double stranded DNA palindrome fragment 5-ACGCGAATTCGCGT-3). The blue color is due to birefringence imaged using cross-polarized light microscopy (magnification, x100).
With the completion of The Cancer Genome Atlas, it is time to evaluate its impact and mine its data to gain a better understanding of cancer biology and therapy.
A study of SIV-infected rhesus macaques suggests that T follicular helper (TFH) cells, a specialized CD4+ T cell subset within the B cell follicles, are a sanctuary for SIV that is largely inaccessible to CD8+ T cells. These findings may open new avenues for research aimed at eradicating HIV.
Pathogenic mutations of the genes encoding isocitrate dehydrogenase 1 (IDH1) and 2 (IDH2) occur in people with acute myeloid leukemia or other tumors. A new study identifies a dependence of IDH-mutated cells on the anti-apoptosis regulator BCL-2 and indicates a 'synthetic lethal' strategy for the treatment of leukemias.
Obesity is a major risk factor for chronic disease. A new study in mice reveals that lowering levels of the signaling molecule serotonin outside of the brain reduces obesity and its complications by increasing brown adipose tissue (BAT) energy expenditure.
Recent studies have suggested that manipulating the tumor-associated macrophage phenotype is a valid therapeutic approach in cancer. In turn, these studies have given some insight into the factors that polarize macrophages, thereby suggesting alternative therapeutic avenues.
Macrophages are responsive to local tissue signals and alter their phenotypes accordingly. In disease tissues this means that macrophage phenotypes may change with disease progression, exacerbating or facilitating the resolution of the pathology.