This week’s articles describe the consequences of preserving pluripotency in cultured stem cells, how glutamate metabolism in T cells contributes to autoimmune disease, and how inactivating BRAF mutations promote tumor growth.
DEVELOPMENT
The costs of preservation
Choi et al. and Yagi et al. report that even short-term preservation of the pluripotency of stem cells in vitro with typical methods using kinase inhibitors alters the expression of genes associated with developmental disorders. In a commentary, Zwaka discusses how these findings raise important and cautionary questions for developmental research and clinical applications.
IMMUNOLOGY
Harnessing immunometabolism to treat autoimmune disease
Xu et al. showed that metabolism epigenetically controls T cell fate and that targeting a glutamate-dependent metabolic pathway may be therapeutic against TH17 cell–mediated autoimmune disease.
CANCER
RAS required for BRAF-inactivated tumors
Yao et al. and Nieto et al. found that inactivating mutations in the kinase BRAF drive tumor growth when coexistent with RAS activation.
