期刊
CANCER DISCOVERY
卷 3, 期 5, 页码 484-486出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/2159-8290.CD-13-0126
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- NCI NIH HHS [CA159859, R01 CA133091, CA163155, CA128583, CA148699, CA102321, CA081403, R01 CA148699, R01 CA102321, U54 CA163155, T32 CA128583, P01 CA081403, R01 CA159859, F32 CA174259, CA133091] Funding Source: Medline
Recurrent mutations in H3F3A at K27 and G34 are frequent in pediatric glioblastoma, but it is unclear how these mutations promote tumorigenesis. In this issue of Cancer Discovery, Bjerke and colleagues identify mutations at G34 in H3F3A that result in elevated expression of MYCN as a potential mechanism in gliomagenesis. Cancer Discov; 3(5); 484-6. (C) 2013 AACR.
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