Abstract：
Vestibular schwannomas (VSs) are benign tumors that develop after biallelic inactivation of the neurofibromatosis type 2 (NF2) gene that encodes the tumor suppressor merlin. Merlin inactivation leads to cell proliferation by dysregulation of receptor tyrosine kinase signaling and other intracellular pathways. In VS without NF2 mutations, dysregulation of non-NF2 genes can promote pathways favoring cell proliferation and tumorigenesis. The tumor microenvironment of VS consists of multiple cell types that influence VS tumor biology through complex intercellular networking and communications.
摘要：
前庭神经鞘瘤（VSs）是良性肿瘤，在编码肿瘤抑制因子merlin的2型神经纤维瘤病（NF2）基因双等位基因失活后发展。Merlin失活通过受体酪氨酸激酶信号传导和其他细胞内途径的失调导致细胞增殖。在没有NF2突变的VS中，非NF2基因的失调可以促进有利于细胞增殖和肿瘤发生的途径。VS的肿瘤微环境由多种细胞类型组成，这些细胞类型通过复杂的细胞间网络和通信影响VS肿瘤生物学。
