Virus-Driven Carcinogenesis
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...
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Veröffentlicht in: | Cancers 2021-05, Vol.13 (11), p.2625 |
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description | 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. |
doi_str_mv | 10.3390/cancers13112625 |
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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.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers13112625</identifier><identifier>PMID: 34071792</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Acquired immune deficiency syndrome ; AIDS ; Carcinogenesis ; Carcinogens ; Cell proliferation ; Cervical cancer ; Classification ; Cytomegalovirus ; DNA damage ; DNA repair ; Epigenetics ; Epstein-Barr virus ; Genes ; Genomes ; Genomic analysis ; Hepatitis ; Hepatitis B ; Hepatitis C ; HIV ; Human immunodeficiency virus ; Human papillomavirus ; Immunosuppression ; Infections ; Insertional mutagenesis ; Latent infection ; Lymphocytes T ; Mutagenesis ; Mutation ; Neck ; Precision medicine ; Review ; Reviews ; Sarcoma ; Tumors ; Viral infections ; Viruses</subject><ispartof>Cancers, 2021-05, Vol.13 (11), p.2625</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c464t-65e0145170651388875535e9e07d3af46f6adccfd79e4fc95df85e37e67d41fd3</citedby><cites>FETCH-LOGICAL-c464t-65e0145170651388875535e9e07d3af46f6adccfd79e4fc95df85e37e67d41fd3</cites><orcidid>0000-0002-1428-1582 ; 0000-0002-5121-6325 ; 0000-0002-5554-8060 ; 0000-0002-3291-0274 ; 0000-0002-7775-4308 ; 0000-0002-1151-2058</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8198641/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8198641/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids></links><search><creatorcontrib>Hatano, Yuichiro</creatorcontrib><creatorcontrib>Ideta, Takayasu</creatorcontrib><creatorcontrib>Hirata, Akihiro</creatorcontrib><creatorcontrib>Hatano, Kayoko</creatorcontrib><creatorcontrib>Tomita, Hiroyuki</creatorcontrib><creatorcontrib>Okada, Hideshi</creatorcontrib><creatorcontrib>Shimizu, Masahito</creatorcontrib><creatorcontrib>Tanaka, Takuji</creatorcontrib><creatorcontrib>Hara, Akira</creatorcontrib><title>Virus-Driven Carcinogenesis</title><title>Cancers</title><description>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). 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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). 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subjects | Acquired immune deficiency syndrome AIDS Carcinogenesis Carcinogens Cell proliferation Cervical cancer Classification Cytomegalovirus DNA damage DNA repair Epigenetics Epstein-Barr virus Genes Genomes Genomic analysis Hepatitis Hepatitis B Hepatitis C HIV Human immunodeficiency virus Human papillomavirus Immunosuppression Infections Insertional mutagenesis Latent infection Lymphocytes T Mutagenesis Mutation Neck Precision medicine Review Reviews Sarcoma Tumors Viral infections Viruses |
title | Virus-Driven Carcinogenesis |
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