Epigenetic analysis in cancer research.

Abstract

The understanding of cancer mechanisms has advanced, revealing the crucial roles of oncogenes, tumor suppressor genes, and epigenetics in cancer progression, making it the second deadliest disease. Genetic changes activating oncogenes and causing uncontrolled cell growth include the Philadelphia chromosome translocation and Ras mutations. Epigenetic alterations like histone modifications and DNA methylation can also disrupt gene regulation in cancer cells. The combination of genetic and epigenetic changes speeds up cancer spread and provides new targets for treatment. Abnormalities in chromatin structure affect gene activity, impacting cellular functions. DNA methylation patterns affect tumor suppressor genes and proto-oncogenes, closely linked to cancer development and spread. DNMT inhibitors, such as Decitabine and Azacytidine, target DNA methylation and show promise in treating certain blood disorders. Non-nucleoside inhibitors are being developed to reduce the toxicity of nucleoside analogs. Cancer treatments focus on histone modifications like acetylation and methylation, crucial for gene control. In has been demonstrated that inhibitors that targets the demethylases and histone methyltransferases stop the proliferation of cancer cells. The FDA has approved HDAC inhibitors such as Panobistat and Vorinostat to trat some types of blood cancer. Novel substances targeting HATs and HDACs, such as PU141 and C646, exhibit inhibitory effects on these enzymes, limiting cancer cell growth. Research is ongoing on natural substances with HDAC inhibitory action, such as apicidin and amamistatin. The effectiveness and safety of the epigenetic cancer treatment are being assessed in the clinical trials. Overall, the potential of epigenetic changes in cancer therapy offers hope for improved outcomes in challenging cancers.