Abstract
H3G34 mutations occur in both pediatric non-brainstem high-grade gliomas (G34R/V) and giant cell tumors of bone (G34W/L). Glioblastoma patients with G34R/V mutation have a generally adverse prognosis, whereas giant cell tumors of bone are rarely metastatic benign tumors. G34 mutations possibly disrupt the epigenome by altering H3K36 modifications, which may involve attenuating the function of SETD2 at methyltransferase. H3K36 methylation change may further lead to genomic instability, dysregulated gene expression pattern, and more mutations. In this chapter, we summarize the pathological features of each mutation type in its respective cancer, as well as the potential mechanism of their disruption on the epigenome and genomic instability. Understanding each mutation type would provide a thorough background for a thorough understanding of the cancers and would bring new insights for future investigations and the development of new precise therapies.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
