Final answer:
Covalent modification of histones can activate oncogenes or inactivate tumor suppressor genes, contributing to cancer progression. Drugs that reverse these epigenetic modifications can restore normal gene expression, aiding in cancer treatment.
Step-by-step explanation:
Covalent modification of histones can lead to either oncogene activation or loss-of-function for a tumor suppressor gene, which plays a significant role in the development and progression of cancer. Histone acetylation and DNA methylation are types of epigenetic modifications that can silence gene expression.
When such modifications occur in histone proteins associated with tumor suppressor genes, it may prevent these genes from performing their normal role in controlling cell growth, leading to uncontrolled proliferation and cancer development.
Conversely, if histone acetylation leads to the overexpression of oncogenes, which are genes that promote cell division and growth, it might contribute to oncogenesis.
Drugs that decrease DNA methylation or inhibit histone deacetylation can reactivate silenced tumor suppressor genes or dampen the activity of oncogenes, thereby helping to restore normal control of cell growth and induce the death of cancer cells.
Understanding the gene expression patterns in cancer cells helps researchers to identify which genes and pathways are disrupted in different cancers, facilitating the development of targeted therapies that can reverse these epigenetic changes and provide personalized treatment strategies.