Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112, USA.
Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, UT 84108, USA; Primary Children's Hospital, Salt Lake City, UT 84113, USA.
Cell Rep. 2024 Aug 27;43(8):114559. doi: 10.1016/j.celrep.2024.114559. Epub 2024 Jul 29.
Medulloblastoma (MB) is the most common malignant brain tumor in children and is stratified into three major subgroups. The Sonic hedgehog (SHH) subgroup represents ∼30% of all MB cases and has significant survival disparity depending upon TP53 status. Here, we describe a zebrafish model of SHH MB using CRISPR to create mutant ptch1, the primary genetic driver of human SHH MB. In these animals, tumors rapidly arise in the cerebellum and resemble human SHH MB by histology and comparative onco-genomics. Similar to human patients, MB tumors with loss of both ptch1 and tp53 have aggressive tumor histology and significantly worse survival outcomes. The simplicity and scalability of the ptch1-crispant MB model makes it highly amenable to CRISPR-based genome-editing screens to identify genes required for SHH MB tumor formation in vivo, and here we identify the gene encoding Grk3 kinase as one such target.
髓母细胞瘤(MB)是儿童中最常见的恶性脑肿瘤,可分为三个主要亚组。Sonic hedgehog(SHH)亚组占所有 MB 病例的约 30%,其生存差异取决于 TP53 状态。在这里,我们使用 CRISPR 技术在斑马鱼中创建了一个 SHH MB 模型,用于创建突变的 ptch1,这是人类 SHH MB 的主要遗传驱动因素。在这些动物中,肿瘤迅速出现在小脑,在组织学和比较肿瘤基因组学上与人类 SHH MB 相似。与人类患者一样,同时缺失 ptch1 和 tp53 的 MB 肿瘤具有侵袭性的肿瘤组织学特征,且生存结果明显较差。ptch1-crispant MB 模型的简单性和可扩展性使其非常适合基于 CRISPR 的全基因组编辑筛选,以鉴定体内形成 SHH MB 肿瘤所需的基因,在这里我们鉴定出编码 Grk3 激酶的基因是这样的一个靶点。