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Published on: January 7, 2019
Epigenetics of Virus-Induced Tumors: Perspectives for Therapeutic Targeting
1NN Blokhin Russian Cancer Research Center, Moscow. Russian Federation.
Abstract:
About 15-20% of human cancers worldwide have viral etiology. Seven human DNA and RNA viruses are accepted to be oncogenic viruses or oncoviruses and contribute to the development of various cancer types. Human oncoviruses have developed multiple molecular mechanisms to interfere with specific cellular pathways to promote viral replication and viral life cycle maintenance in the host. Despite the diversity of oncogenic viruses, they use similar strategies for cancer development. Viral oncoproteins and viral non-coding RNAs are the key factors that can affect multiple cellular processes on both genetic and epigenetic levels. Epigenetics research allows better understanding of the complex interplay between oncoviruses and the host cells. This review highlights the importance of epigenetic reprogramming for virus-induced carcinogenesis. Recent progress in the development of pharmacological tools for targeting epigenetic mechanisms opens new perspectives for modulation of virus/host interaction and intervention of virus-induced cancer. Several clinical trials have been carried out or are on-going involving epigenetic drugs not only as single therapeutic but also in combination with other targeted agents against various virus-induced cancers.
Insights
Human oncoviruses, or cancer-causing viruses, contribute to 15-20% of global cancers. Epigenetic reprogramming is key to understanding and treating virus-induced cancers with new drug therapies.
Area of Science:
- Oncology
- Virology
- Epigenetics
Background:
- Approximately 15-20% of human cancers globally are linked to viral infections.
- Seven human DNA and RNA viruses, known as oncoviruses, are recognized carcinogens contributing to diverse cancer types.
- Oncoviruses employ sophisticated molecular strategies, including viral oncoproteins and non-coding RNAs, to manipulate host cellular pathways for replication and survival.
Purpose of the Study:
- To review the critical role of epigenetic reprogramming in virus-induced carcinogenesis.
- To explore how understanding the interplay between oncoviruses and host epigenetics can inform cancer intervention strategies.
- To highlight advancements in epigenetic pharmacological tools for modulating virus-host interactions and treating virus-associated cancers.
Main Methods:
- Literature review focusing on molecular mechanisms of oncoviruses.
- Analysis of epigenetic alterations in virus-induced cancers.
- Examination of current and ongoing clinical trials involving epigenetic drugs for viral cancers.
Main Results:
- Oncoviruses utilize common strategies to induce cancer, affecting cellular processes at genetic and epigenetic levels.
- Epigenetics provides crucial insights into the complex interactions between oncoviruses and host cells.
- Progress in epigenetic drug development offers new therapeutic avenues for virus-induced cancers.
Conclusions:
- Epigenetic reprogramming is a central mechanism in virus-induced carcinogenesis.
- Targeting epigenetic modifications presents promising strategies for novel cancer therapies.
- Clinical trials investigating epigenetic drugs show potential for treating various virus-associated cancers, often in combination therapies.
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