Molecular epigenetics and genetics in neuro-oncology

摘要: Gliomas arise through genetic and epigenetic alterations of normal brain cells, although the exact cell origin for each glioma subtype is unknown. The alteration-induced changes in gene expression protein function allow uncontrolled division, tumor expansion, infiltration into surrounding parenchyma. are tumor-grade specific. Particular predict aggressiveness, response to therapy, patient survival. Genetic include deletion, gain, amplification, mutation, translocation, which result oncogene activation suppressor inactivation, or some instances may simply be a consequence tumorigenesis. Epigenetic tumors CpG island hypermethylation associated with silencing, gene-specific hypomethylation aberrant activation, genome-wide potentially leading loss imprinting, chromosomal instability, cellular hyperproliferation. Other alterations, such as position histone variants modifications also likely important molecular pathology tumors. Given that deacetylases targets drugs already clinical trial, surprisingly little known about acetylation primary Although majority independent there interaction on specific genes, signaling pathways within domains. Next-generation sequencing technology now method choice genomic epigenome profiling, allowing more comprehensive understanding contributions tumorigenesis brain.