Because the degree of DNA methylation appears to be a relatively reliable genetic marker for some forms of cancer, researchers have explored the possibility of altering DNA methylation as a form of cancer therapy. Initial studies indicate that while hypomethylation suppresses the formation of some tumors, other tumors thrive. Why would one expect different cancers to respond differently to either hypomethylation or hypermethylation therapies?

Key Concepts

DNA Methylation

DNA methylation is a biochemical process involving the addition of a methyl group to the DNA molecule, typically at cytosine bases. This modification can regulate gene expression without altering the underlying DNA sequence, influencing cellular functions and development. In cancer, abnormal methylation patterns can lead to the silencing of tumor suppressor genes or activation of oncogenes, contributing to tumorigenesis.

Tumor Heterogeneity

Tumor heterogeneity refers to the diverse genetic and phenotypic variations observed within and between tumors. This variability can arise from differences in genetic mutations, epigenetic modifications, and microenvironmental factors. As a result, different cancer types or even subtypes of the same cancer may respond differently to treatments targeting methylation, making personalized approaches essential in cancer therapy.

Epigenetic Therapy

Epigenetic therapy involves the use of drugs or interventions to modify epigenetic marks, such as DNA methylation, to restore normal gene function in cancer cells. These therapies can either inhibit methylation (hypomethylation) to reactivate silenced genes or promote methylation (hypermethylation) to silence overactive oncogenes. The effectiveness of these therapies can vary significantly among different cancers due to their unique epigenetic landscapes.