BRAF Mutations Open Doors for N-Ethyl-N-Nitrosourea-Induced Gliomagenesis.
BRAF Mutations Open Doors for N-Ethyl-N-Nitrosourea-Induced Gliomagenesis.
复制标题
DOI:
10.1016/j.ajpath.2016.07.005
复制
发表时间:
2016-10
期刊:
影响因子:
--
通讯作者:
R. S. McNeill;David M. Irvin;C. Miller
中科院分区:
文献类型:
--
作者:
R. S. McNeill;David M. Irvin;C. Miller
In this issue of the American Journal of Pathology, Wang et al 1 identified recurrent Braf mutations in N-ethyl-N-nitrosourea (ENU)–induced rat gliomas by DNA sequencing. Their results provide a platform for preclinical development of novel targeted therapies for BRAF-mutant gliomas. Precision oncology promises to revolutionize cancer therapy by stratifying tumors on the basis of their molecular characteristics and using rationally designed treatments in molecularly defined patient populations. 2 Although the field of oncology is transitioning into the precision medicine era, conventional diagnostics, based on tissue type, tumor pathology, and patient demographics, remain essential to quality care. One natural pathological division for gliomas, the most common primary brain tumors in humans, is based on their invasion, with nondiffuse gliomas forming well-circumscribed tumors and diffuse gliomas invading the normal brain. 3 Within these two broad diagnostic categories, gliomas are further subdivided on the basis of patient demographics into pediatric and adult diseases and further into specific diagnostic entities based on their histological appearance.