抑制 ERK/MAPK 信号通路可能成为预防 1 型神经纤维瘤病婴儿视神经通路胶质瘤的一种治疗方法。

Inhibition of ERK/MAPK signaling as potential therapy to prevent optic pathway glioma in infants with neurofibromatosis type 1.

机构信息

Institute for Cancer Genetics, Columbia University Medical Center, New York, NY 10032, USA.

Institute for Cancer Genetics, Columbia University Medical Center, New York, NY 10032, USA; Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY 10032, USA; Department of Pediatrics, Columbia University Medical Center, New York, NY 10032, USA; Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, NY 10032, USA.

出版信息

Dev Cell. 2021 Oct 25;56(20):2785-2786. doi: 10.1016/j.devcel.2021.10.001.

DOI:10.1016/j.devcel.2021.10.001

PMID:34699786

Abstract

Pediatric low-grade gliomas (pLGGs) arise primarily at early stages of development. The molecular mechanisms of pLGG gliomagenesis are unclear, as is the progenitor cell of origin. In this issue of Developmental Cell, Jecrois et al. show that NF1-associated optic pathway gliomas originate from migrating glial progenitors that have distinct MEK/ERK dependency.

摘要

小儿低度恶性神经胶质瘤（pLGGs）主要发生在发育早期。pLGG 发生的分子机制尚不清楚，起源前体细胞也是如此。在本期《发育细胞》中，Jecrois 等人表明，NF1 相关视神经通路胶质瘤起源于具有独特 MEK/ERK 依赖性的迁移神经胶质前体细胞。