University of California San Francisco, San Francisco, CA, USA.
Cancer Discov. 2013 May;3(5):484-6. doi: 10.1158/2159-8290.CD-13-0126.
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.
在儿童脑胶质瘤中，H3F3A 中的 K27 和 G34 频繁出现复发突变，但这些突变如何促进肿瘤发生尚不清楚。在本期《癌症发现》杂志中，Bjerke 及其同事鉴定出 H3F3A 中的 G34 突变导致 MYCN 表达升高，这可能是胶质瘤发生的一种潜在机制。
