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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA
Published on: December 19, 2019
Virus-Driven Carcinogenesis
Yuichiro Hatano1, Takayasu Ideta2,3, Akihiro Hirata4
1Department of Tumor Pathology, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan.
Abstract:
Cancer arises from the accumulation of genetic and epigenetic alterations. Even in the era of precision oncology, carcinogens contributing to neoplastic process are still an important focus of research. Comprehensive genomic analyses have revealed various combinations of base substitutions, referred to as the mutational signatures, in cancer. Each mutational signature is believed to arise from specific DNA damage and repair processes, including carcinogens. However, as a type of carcinogen, tumor viruses increase the cancer risk by alternative mechanisms, including insertional mutagenesis, viral oncogenes, and immunosuppression. In this review, we summarize virus-driven carcinogenesis to provide a framework for the control of malignant cell proliferation. We first provide a brief overview of oncogenic viruses and describe their implication in virus-related tumors. Next, we describe tumor viruses (HPV, Human papilloma virus; HBV, Hepatitis B virus; HCV, Hepatitis C virus; EBV, Epstein-Barr virus; Kaposi sarcoma herpesvirus; MCV, Merkel cell polyoma virus; HTLV-1, Human T-cell lymphotropic virus, type-1) and tumor virus-related cancers. Lastly, we introduce emerging tumor virus candidates, human cytomegalovirus (CMV), human herpesvirus-6 (HHV-6) and adeno-associated virus-2 (AAV-2). We expect this review to be a hub in a complex network of data for virus-associated carcinogenesis.
Insights
This review explores how tumor viruses cause cancer through mechanisms like insertional mutagenesis and viral oncogenes, offering a framework for controlling malignant cell growth. It details known oncogenic viruses and emerging candidates involved in virus-driven carcinogenesis.
Area of Science:
- Oncology
- Virology
- Genetics
Background:
- Cancer develops from genetic and epigenetic changes, with carcinogens playing a key role.
- While mutational signatures from DNA damage are studied, tumor viruses represent a distinct class of carcinogens.
- Tumor viruses contribute to cancer through insertional mutagenesis, viral oncogenes, and immunosuppression.
Purpose of the Study:
- To review virus-driven carcinogenesis and establish a framework for controlling malignant cell proliferation.
- To provide an overview of oncogenic viruses and their association with various tumors.
- To highlight known and emerging viral candidates implicated in cancer development.
Main Methods:
- Literature review of oncogenic viruses and their mechanisms.
- Summarization of established tumor viruses (HPV, HBV, HCV, EBV, KSHV, MCV, HTLV-1) and associated cancers.
- Introduction of emerging viral candidates (CMV, HHV-6, AAV-2).
Main Results:
- Identified specific tumor viruses and their roles in different cancers.
- Described alternative carcinogenic mechanisms employed by viruses beyond DNA damage.
- Highlighted emerging viral candidates with potential oncogenic activity.
Conclusions:
- Virus-driven carcinogenesis is a significant factor in cancer development.
- Understanding viral mechanisms is crucial for developing strategies to control virus-associated cancers.
- This review serves as a central resource for data on virus-associated carcinogenesis.
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