A brief survey of health habits among childhood cancer survivors.

Using a survey, we assessed four health habits in 468 pediatric cancer survivors. Approximately 75% were at goal for ≥1 behavior-44% were active ≥1 hr per day, 40% engaged in ≤1 hr of screen time a day, 34% consumed sweetened beverages not often, and 4% ate >4 servings of fruits and vegetables per day. Survivors' age was associated with being active (P < 0.001) and limited screen time (P = 0.001). Males were more likely to be active (P = 0.003). The most common combination of goal behaviors was activity and screen time. Encouraging healthy behaviors may decrease the burden of late effects in survivors.

Gcn5 loss-of-function accelerates cerebellar and retinal degeneration in a SCA7 mouse model.

Spinocerebellar ataxia type 7 (SCA7) is a neurodegenerative disease caused by expansion of a CAG repeat encoding a polyglutamine tract in ATXN7, a component of the SAGA histone acetyltransferase (HAT) complex. Previous studies provided conflicting evidence regarding the effects of polyQ-ATXN7 on the activity of Gcn5, the HAT catalytic subunit of SAGA. Here, we report that reducing Gcn5 expression accelerates both cerebellar and retinal degeneration in a mouse model of SCA7. Deletion of Gcn5 in Purkinje cells in mice expressing wild-type (wt) Atxn7, however, causes only mild ataxia and does not lead to the early lethality observed in SCA7 mice. Reduced Gcn5 expression strongly enhances retinopathy in SCA7 mice, but does not affect the known transcriptional targets of Atxn7, as expression of these genes is not further altered by Gcn5 depletion. These findings demonstrate that loss of Gcn5 functions can contribute to the time of onset and severity of SCA7 phenotypes, and suggest that non-transcriptional functions of SAGA may play a role in neurodegeneration in this disease.