DNA hypomethylation |
Activation of cellular oncogenes |
Increased proliferation, growth advantage |
|
Activation of transposable element |
Genomic instability, transcriptional noise |
DNA hypermethylation |
De novo hypermethylation of CpG islands within gene promoters leading to silencing of tumor suppressors and cancer-associated genes |
Genomic and chromosomal instability, increased proliferation, growth advantage |
Loss of imprinting (LOI) |
Reactivation of silent alleles, biallelic expression of imprinted genes |
Expansion of precursor cell population |
Relaxation of X-chromosome inactivation |
Mechanisms is unknown but it appears to be age-related |
Altered gene dosage, growth advantage |
Histone acetylation |
Gain-of-function |
Activation of tumor promoting genes |
|
Loss-of-function |
Defects in DNA repair and checkpoints |
Histone deacetylation |
Silencing of tumor suppressor genes |
Genomic instability, increased proliferation |
Histone methylation |
Loss of heritable patterns of gene expression (“cellular memory”) |
Genomic instability, growth advantage |
MicroRNAs (miRNAs) amplification in cancer |
Function as oncogenes |
Neoplastic transformation |
MicroRNAs (miRNAs) deletion in cancer |
Function as tumor suppressors. |
Neoplastic transformation |