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Journal articles on the topic 'Viral carcinogenesis'

To see the other types of publications on this topic, follow the link: Viral carcinogenesis.

Author: Grafiati

Published: 4 June 2021

Last updated: 2 March 2023

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1

Wyke, J. A. "Viral carcinogenesis — illustrated introductory thoughts." European Journal of Cancer and Clinical Oncology 23, no. 11 (November 1987): 1813. http://dx.doi.org/10.1016/0277-5379(87)90768-1.

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2

Jain, Sidhant, Madhumita Sengupta, and Pooja Jain. "Non-Viral Parasites Associated with Carcinogenesis." Cancer Investigation 37, no. 9 (September 13, 2019): 453–62. http://dx.doi.org/10.1080/07357907.2019.1662918.

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3

Mayer, V., and P. Ebbesen. "Persistent viral infections in human carcinogenesis." European Journal of Cancer Prevention 3, no. 1 (January 1994): 5–14. http://dx.doi.org/10.1097/00008469-199401000-00002.

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4

Badawi, H., H. Ahmed, A. Ismail, N. El-Khafif, A. Helmy, A. Badawy, S. Mansy, and M. Saber. "R2309 Bladder carcinogenesis via viral infection." International Journal of Antimicrobial Agents 29 (March 2007): S669. http://dx.doi.org/10.1016/s0924-8579(07)72148-9.

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5

Elkhalifa, Ahmed M. E., Showkat Ul Nabi, Ovais Shabir Shah, Showkeen Muzamil Bashir, Umar Muzaffer, Sofi Imtiyaz Ali, Imtiyaz Ahmad Wani, et al. "Insight into Oncogenic Viral Pathways as Drivers of Viral Cancers: Implication for Effective Therapy." Current Oncology 30, no. 2 (February 5, 2023): 1924–44. http://dx.doi.org/10.3390/curroncol30020150.

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As per a recent study conducted by the WHO, 15.4% of all cancers are caused by infectious agents of various categories, and more than 10% of them are attributed to viruses. The emergence of COVID-19 has once again diverted the scientific community’s attention toward viral diseases. Some researchers have postulated that SARS-CoV-2 will add its name to the growing list of oncogenic viruses in the long run. However, owing to the complexities in carcinogenesis of viral origin, researchers across the world are struggling to identify the common thread that runs across different oncogenic viruses. Classical pathways of viral oncogenesis have identified oncogenic mediators in oncogenic viruses, but these mediators have been reported to act on diverse cellular and multiple omics pathways. In addition to viral mediators of carcinogenesis, researchers have identified various host factors responsible for viral carcinogenesis. Henceforth owing to viral and host complexities in viral carcinogenesis, a singular mechanistic pathway remains yet to be established; hence there is an urgent need to integrate concepts from system biology, cancer microenvironment, evolutionary perspective, and thermodynamics to understand the role of viruses as drivers of cancer. In the present manuscript, we provide a holistic view of the pathogenic pathways involved in viral oncogenesis with special emphasis on alteration in the tumor microenvironment, genomic alteration, biological entropy, evolutionary selection, and host determinants involved in the pathogenesis of viral tumor genesis. These concepts can provide important insight into viral cancers, which can have an important implication for developing novel, effective, and personalized therapeutic options for treating viral cancers.

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6

Kamalov, A. A., L. M. Mikhaleva, V. B. Matveev, V. K. Karpov, D. A. Okhobotov, O. A. Osmanov, E. P. Akopyan, and B. M. Shaparov. "Viral infections in prostate carcinogenesis: literature review." Cancer Urology 18, no. 2 (August 14, 2022): 182–89. http://dx.doi.org/10.17650/1726-9776-2022-18-2-182-189.

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Prostate cancer is one of the most common malignant diseases in men. Viral infections can be risk factors for prostate carcinogenesis. Based on the literature review, an assumption can be made about the pathogenetic role of viral infections in prostate carcinogenesis. Further study of this problem is required, the solution of which can make a great contribution to the diagnosis and prevention of prostate cancer

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7

Honda, Masao, and Shuichi Kaneko. "1. Hepatic Carcinogenesis Associated with Viral Hepatitis." Nihon Naika Gakkai Zasshi 97, no. 1 (2008): 82–91. http://dx.doi.org/10.2169/naika.97.82.

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8

Harikumar, Kuzhuvelil B., Girija Kuttan, and Ramadasan Kuttan. "Inhibition of Viral Carcinogenesis by Phyllanthus amarus." Integrative Cancer Therapies 8, no. 3 (August 11, 2009): 254–60. http://dx.doi.org/10.1177/1534735409340162.

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9

Flaitz, C. M., and M. J. Hicks. "Molecular piracy: the viral link to carcinogenesis." Oral Oncology 34, no. 6 (November 1998): 448–53. http://dx.doi.org/10.1016/s1368-8375(98)00057-8.

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10

Ryu, Wang-Shick. "Molecular Aspects of Hepatitis B Viral Infection and the Viral Carcinogenesis." BMB Reports 36, no. 1 (January 31, 2003): 138–43. http://dx.doi.org/10.5483/bmbrep.2003.36.1.138.

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11

Scott, Martin L., Henry S. Kaplan, Mark B. Feinberg, Marilyn Travis, and Miriam Lieberman. "Viral and radiation carcinogenesis of C57BL/Ka mice." Leukemia Research 10, no. 7 (January 1986): 775. http://dx.doi.org/10.1016/0145-2126(86)90296-1.

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12

Georgakilas, Alexandros G., William G. Mosley, Stavroula Georgakila, Dominique Ziech, and Mihalis I. Panayiotidis. "Viral-induced human carcinogenesis: an oxidative stress perspective." Molecular BioSystems 6, no. 7 (2010): 1162. http://dx.doi.org/10.1039/b923958h.

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13

Gallo, Alessia, Vitale Miceli, Matteo Bulati, Gioacchin Iannolo, Flavia Contino, and Pier Giulio Conaldi. "Viral miRNAs as Active Players and Participants in Tumorigenesis." Cancers 12, no. 2 (February 4, 2020): 358. http://dx.doi.org/10.3390/cancers12020358.

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The theory that viruses play a role in human cancers is now supported by scientific evidence. In fact, around 12% of human cancers, a leading cause of morbidity and mortality in some regions, are attributed to viral infections. However, the molecular mechanism remains complex to decipher. In recent decades, the uncovering of cellular miRNAs, with their invaluable potential as diagnostic and prognostic biomarkers, has increased the number of studies being conducted regarding human cancer diagnosis. Viruses develop clever mechanisms to succeed in the maintenance of the viral life cycle, and some viruses, especially herpesviruses, encode for miRNA, v-miRNAs. Through this viral miRNA, the viruses are able to manipulate cellular and viral gene expression, driving carcinogenesis and escaping the host innate or adaptive immune system. In this review, we have discussed the main viral miRNAs and virally influenced cellular pathways, and their capability to drive carcinogenesis.

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14

Palrasu, Manikandan, Elena Zaika, Wael El-Rifai, Jianwen Que, and Alexander I. Zaika. "Role of Bacterial and Viral Pathogens in Gastric Carcinogenesis." Cancers 13, no. 8 (April 14, 2021): 1878. http://dx.doi.org/10.3390/cancers13081878.

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Gastric cancer (GC) is one of the deadliest malignancies worldwide. In contrast to many other tumor types, gastric carcinogenesis is tightly linked to infectious events. Infections with Helicobacter pylori (H. pylori) bacterium and Epstein–Barr virus (EBV) are the two most investigated risk factors for GC. These pathogens infect more than half of the world’s population. Fortunately, only a small fraction of infected individuals develops GC, suggesting high complexity of tumorigenic processes in the human stomach. Recent studies suggest that the multifaceted interplay between microbial, environmental, and host genetic factors underlies gastric tumorigenesis. Many aspects of these interactions still remain unclear. In this review, we update on recent discoveries, focusing on the roles of various gastric pathogens and gastric microbiome in tumorigenesis.

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15

Chen, Yan, Vonetta Williams, Maria Filippova, Valery Filippov, and Penelope Duerksen-Hughes. "Viral Carcinogenesis: Factors Inducing DNA Damage and Virus Integration." Cancers 6, no. 4 (October 22, 2014): 2155–86. http://dx.doi.org/10.3390/cancers6042155.

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16

Lizano, Marcela, Jaime Berumen, and Alejandro García-Carrancá. "HPV-related Carcinogenesis: Basic Concepts, Viral Types and Variants." Archives of Medical Research 40, no. 6 (August 2009): 428–34. http://dx.doi.org/10.1016/j.arcmed.2009.06.001.

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17

Foppoli, Cesira, Federico De Marco, Chiara Cini, and M. Perluigi. "Redox control of viral carcinogenesis: The human papillomavirus paradigm." Biochimica et Biophysica Acta (BBA) - General Subjects 1850, no. 8 (August 2015): 1622–32. http://dx.doi.org/10.1016/j.bbagen.2014.12.016.

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18

Schirmacher, Peter, Charles E. Rogler, and Hans P. Dienes. "Current pathogenetic and molecular concepts in viral liver carcinogenesis." Virchows Archiv B Cell Pathology Including Molecular Pathology 63, no. 1 (December 1993): 71–89. http://dx.doi.org/10.1007/bf02899246.

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19

Hatano, Yuichiro, Takayasu Ideta, Akihiro Hirata, Kayoko Hatano, Hiroyuki Tomita, Hideshi Okada, Masahito Shimizu, Takuji Tanaka, and Akira Hara. "Virus-Driven Carcinogenesis." Cancers 13, no. 11 (May 27, 2021): 2625. http://dx.doi.org/10.3390/cancers13112625.

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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.

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20

Sharma, Mohit, Madhusudan Astekar, Sonal Soi, Bhari Manjunatha, and Devi Shetty. "Viral Carcinogenesis of Oral Region and Recent Trends in Treatment." Recent Patents on Biomarkers 5, no. 1 (June 8, 2015): 25–34. http://dx.doi.org/10.2174/2210309005666150505183429.

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21

Bharti, Alok Chandra. "miRNA as viral transcription tuners in HPV-mediated cervical carcinogenesis." Frontiers in Bioscience 10, no. 1 (2018): 21–47. http://dx.doi.org/10.2741/s499.

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22

Park, N. H., E. Akoto-Amanfu, and D. I. Paik. "Smokeless Tobacco Carcinogenesis: The Role of Viral and Other Factors." CA: A Cancer Journal for Clinicians 38, no. 4 (July 1, 1988): 248–56. http://dx.doi.org/10.3322/canjclin.38.4.248.

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23

Elpek, Gulsum Ozlem. "Molecular pathways in viral hepatitis-associated liver carcinogenesis: An update." World Journal of Clinical Cases 9, no. 19 (July 6, 2021): 4890–917. http://dx.doi.org/10.12998/wjcc.v9.i19.4890.

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24

Cuninghame, Sean, Robert Jackson, and Ingeborg Zehbe. "Hypoxia-inducible factor 1 and its role in viral carcinogenesis." Virology 456-457 (May 2014): 370–83. http://dx.doi.org/10.1016/j.virol.2014.02.027.

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25

Pinheiro, Maisa, Ariana Harari, Mark Schiffman, Gary M. Clifford, Zigui Chen, Meredith Yeager, Michael Cullen, et al. "Phylogenomic Analysis of Human Papillomavirus Type 31 and Cervical Carcinogenesis: A Study of 2093 Viral Genomes." Viruses 13, no. 10 (September 28, 2021): 1948. http://dx.doi.org/10.3390/v13101948.

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Human papillomavirus (HPV) type 31 (HPV31) is closely related to the most carcinogenic type, HPV16, but only accounts for 4% of cervical cancer cases worldwide. Viral genetic and epigenetic variations have been associated with carcinogenesis for other high-risk HPV types, but little is known about HPV31. We sequenced 2093 HPV31 viral whole genomes from two large studies, one from the U.S. and one international. In addition, we investigated CpG methylation in a subset of 175 samples. We evaluated the association of HPV31 lineages/sublineages, single nucleotide polymorphisms (SNPs) and viral methylation with cervical carcinogenesis. HPV31 A/B clade was >1.8-fold more associated with cervical intraepithelial neoplasia grade 3 and cancer (CIN3+) compared to the most common C lineage. Lineage/sublineage distribution varied by race/ethnicity and geographic region. A viral genome-wide association analysis identified SNPs within the A/B clade associated with CIN3+, including H23Y (C626T) (odds ratio = 1.60, confidence intervals = 1.17–2.19) located in the pRb CR2 binding-site within the E7 oncogene. Viral CpG methylation was higher in lineage B, compared to the other lineages, and was most elevated in CIN3+. In conclusion, these data support the increased oncogenicity of the A/B lineages and suggest variation of E7 as a contributing risk factor.

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26

Rajeev, R., Kanaram Choudhary, Swagatika Panda, and Neha Gandhi. "Role of bacteria in oral carcinogenesis." South Asian Journal of Cancer 01, no. 02 (October 2012): 78–83. http://dx.doi.org/10.4103/2278-330x.103719.

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AbstractOral cancer is the most common cancer diagnosed in Indian men and is the leading cause of cancer deaths. It is considered as a multistep and multifactorial disease. Besides accumulation of genetic mutations, numerous other carcinogens are involved. In this category, viral and chemical carcinogens are well studied and documented. However, in the oral cavity, the role of microbiota in carcinogenesis is not known. Microbial populations on mouth mucosa differ between healthy and malignant sites, and certain oral bacterial species have been linked with malignancies, but the evidence is still weak in this respect. Nevertheless, oral microorganisms inevitably up-regulate cytokines and other inflammatory mediators that affect the complex metabolic pathways, and may thus be involved in carcinogenesis. Poor oral health associates statistically with prevalence of many types of cancer such as pancreatic and gastrointestinal cancer. This review presents possible carcinogenesis pathway involved in bacterial carcinogenesis, commonly implicated bacteria in oral carcinogenesis, and their role in cancer therapeutics as well.

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27

Lewis, A., and J. Cook. "A new role for DNA virus early proteins in viral carcinogenesis." Science 227, no. 4682 (January 4, 1985): 15–20. http://dx.doi.org/10.1126/science.3843807.

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28

Huleihel, Mahmoud, Ahmad Salman, Vitaly Erukhimovitch, Jagannathan Ramesh, Ziad Hammody, and Shaul Mordechai. "Novel spectral method for the study of viral carcinogenesis in vitro." Journal of Biochemical and Biophysical Methods 50, no. 2-3 (January 2002): 111–21. http://dx.doi.org/10.1016/s0165-022x(01)00177-4.

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29

Butel, Janet S. "Viral carcinogenesis: revelation of molecular mechanisms and etiology of human disease." Carcinogenesis 21, no. 3 (March 2000): 405–26. http://dx.doi.org/10.1093/carcin/21.3.405.

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30

Pitha-Rowe, Ian F., and Paula M. Pitha. "Viral defense, carcinogenesis and ISG15: Novel roles for an old ISG." Cytokine & Growth Factor Reviews 18, no. 5-6 (October 2007): 409–17. http://dx.doi.org/10.1016/j.cytogfr.2007.06.017.

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31

Della Fera, Ashley N., Alix Warburton, Tami L. Coursey, Simran Khurana, and Alison A. McBride. "Persistent Human Papillomavirus Infection." Viruses 13, no. 2 (February 20, 2021): 321. http://dx.doi.org/10.3390/v13020321.

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Persistent infection with oncogenic human papillomavirus (HPV) types is responsible for ~5% of human cancers. The HPV infectious cycle can sustain long-term infection in stratified epithelia because viral DNA is maintained as low copy number extrachromosomal plasmids in the dividing basal cells of a lesion, while progeny viral genomes are amplified to large numbers in differentiated superficial cells. The viral E1 and E2 proteins initiate viral DNA replication and maintain and partition viral genomes, in concert with the cellular replication machinery. Additionally, the E5, E6, and E7 proteins are required to evade host immune responses and to produce a cellular environment that supports viral DNA replication. An unfortunate consequence of the manipulation of cellular proliferation and differentiation is that cells become at high risk for carcinogenesis.

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32

Heredia-Torres, Tania Guadalupe, Ana Rosa Rincón-Sánchez, Sonia Amelia Lozano-Sepúlveda, Kame Galan-Huerta, Daniel Arellanos-Soto, Marisela García-Hernández, Aurora de Jesús Garza-Juarez, and Ana María Rivas-Estilla. "Unraveling the Molecular Mechanisms Involved in HCV-Induced Carcinogenesis." Viruses 14, no. 12 (December 11, 2022): 2762. http://dx.doi.org/10.3390/v14122762.

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Cancer induced by a viral infection is among the leading causes of cancer. Hepatitis C Virus (HCV) is a hepatotropic oncogenic positive-sense RNA virus that leads to chronic infection, exposing the liver to a continuous process of damage and regeneration and promoting hepatocarcinogenesis. The virus promotes the development of carcinogenesis through indirect and direct molecular mechanisms such as chronic inflammation, oxidative stress, steatosis, genetic alterations, epithelial-mesenchymal transition, proliferation, and apoptosis, among others. Recently, direct-acting antivirals (DAAs) showed sustained virologic response in 95% of cases. Nevertheless, patients treated with DAAs have reported an unexpected increase in the early incidence of Hepatocellular carcinoma (HCC). Studies suggest that HCV induces epigenetic regulation through non-coding RNAs, DNA methylation, and chromatin remodeling, which modify gene expressions and induce genomic instability related to HCC development that persists with the infection’s clearance. The need for a better understanding of the molecular mechanisms associated with the development of carcinogenesis is evident. The aim of this review was to unravel the molecular pathways involved in the development of carcinogenesis before, during, and after the viral infection’s resolution, and how these pathways were regulated by the virus, to find control points that can be used as potential therapeutic targets.

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33

Zivadinovic, Radomir, Aleksandra Petric, Goran Lilic, Vekoslav Lilic, and Biljana Djordjevic. "Persistent human papillomavirus infection in the etiology of cervical carcinoma: The role of immunological, genetic, viral and cellular factors." Srpski arhiv za celokupno lekarstvo 142, no. 5-6 (2014): 378–83. http://dx.doi.org/10.2298/sarh1406378z.

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The aim of this paper was to present the role of human papillomavirus (HPV) in cervical carcinogenesis from several aspects. By explaining the HPV virus lifecycle and structure, its effect on cervical cell cycle and subversion of immune response can be better understood. Early E region of the viral genome encodes proteins that are directly involved in carcinogenesis. The E6 protein binds to p53 protein (product of tumor-suppressor gene) blocking and degrading it, which in turn prevents cell cycle arrest and apoptosis induction. E6 is also capable of telomerase activation, which leads to cell immortalization; it also reacts with host proto-oncogene c-jun, responsible for transcription, shortens G1 phase and speeds up the transition from G1 to S phase of the cells infected by HPV. E7 forms bonds with retinoblastoma protein (product of tumor-suppressor gene) and inactivates it. It can inactivate cyclin inhibitors p21, p27, and abrogate the mitotic spindle checkpoint with the loss of protective effect of pRB and p53. The immune system cannot initiate early immunological reaction since the virus is non-lytic, while the concentration of viral proteins - antigens is low and has a basal intracellular position. Presentation through Langerhans cells (LC) is weak, because the number of these cells is low due to the effect of HPV. E7 HPV reduces the expression of E-cadherin, which is responsible for LC adhesion to HPVtransformed keratinocytes. Based on these considerations, it may be concluded that the process of cervical carcinogenesis includes viral, genetic, cellular, molecular-biological, endocrine, exocrine and immunological factors.

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34

Manole, Bianca, Costin Damian, Simona-Eliza Giusca, Irina Draga Caruntu, Elena Porumb-Andrese, Catalina Lunca, Olivia Simona Dorneanu, Luminita Smaranda Iancu, and Ramona Gabriela Ursu. "The Influence of Oncogenic Viruses in Renal Carcinogenesis: Pros and Cons." Pathogens 11, no. 7 (July 2, 2022): 757. http://dx.doi.org/10.3390/pathogens11070757.

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Viral infections are major contributors to the global cancer burden. Recent advances have revealed that known oncogenic viruses promote carcinogenesis through shared host cell targets and pathways. The aim of this review is to point out the connection between several oncogenic viruses from the Polyomaviridae, Herpesviridae and Flaviviridae families and renal carcinogenesis, highlighting their involvement in the carcinogenic mechanism. We performed a systematic search of the PubMed and EMBASE databases, which was carried out for all the published studies on RCC in the last 10 years, using the following search algorithm: renal cell carcinoma (RCC) and urothelial carcinoma, and oncogenic viruses (BKPyV, EBV, HCV, HPV and Kaposi Sarcoma Virus), RCC and biomarkers, immunohistochemistry (IHC). Our analysis included studies that were published in English from the 1st of January 2012 to the 1st of May 2022 and that described and analyzed the assays used for the detection of oncogenic viruses in RCC and urothelial carcinoma. The virus most frequently associated with RCC was BKPyV. This review of the literature will help to understand the pathogenic mechanism of the main type of renal malignancy and whether the viral etiology can be confirmed, at a minimum, as a co-factor. In consequence, these data can contribute to the development of new therapeutic strategies. A virus-induced tumor could be efficiently prevented by vaccination or treatment with oncolytic viral therapy and/or by targeted therapy.

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35

Stenbäck, Frej, Gary Curtis, and Allan J. Jacobs. "Viral agents in two-stage cervical carcinogenesis: An experimental study in mice." Gynecologic Oncology 32, no. 2 (February 1989): 218–23. http://dx.doi.org/10.1016/s0090-8258(89)80036-8.

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36

Elgui de Oliveira, Deilson, Bárbara G. Müller-Coan, and Joseph S. Pagano. "Viral Carcinogenesis Beyond Malignant Transformation: EBV in the Progression of Human Cancers." Trends in Microbiology 24, no. 8 (August 2016): 649–64. http://dx.doi.org/10.1016/j.tim.2016.03.008.

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37

IKEDA, K. "P-502 Influence of interferon administration on hepatocellular carcinogenesis from viral cirrhosis." International Hepatology Communications 3 (July 1995): S162. http://dx.doi.org/10.1016/0928-4346(95)90797-b.

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38

Kremsdorf, D., P. Soussan, P. Paterlini-Brechot, and C. Brechot. "Hepatitis B virus-related hepatocellular carcinoma: paradigms for viral-related human carcinogenesis." Oncogene 25, no. 27 (June 2006): 3823–33. http://dx.doi.org/10.1038/sj.onc.1209559.

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39

Vázquez-Ulloa, Elenaé, Marcela Lizano, Marika Sjöqvist, Leslie Olmedo-Nieva, and Adriana Contreras-Paredes. "Deregulation of the Notch pathway as a common road in viral carcinogenesis." Reviews in Medical Virology 28, no. 5 (June 28, 2018): e1988. http://dx.doi.org/10.1002/rmv.1988.

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40

Guo, Ju-Tao, and Timothy M. Block. "Do hepatitis B virus surface antigens have any role in viral carcinogenesis?" Hepatology 68, no. 3 (July 16, 2018): 801–3. http://dx.doi.org/10.1002/hep.29886.

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41

Morel, Adeline, Cindy Neuzillet, Maxime Wack, Sonia Lameiras, Sophie Vacher, Marc Deloger, Nicolas Servant, et al. "Mechanistic Signatures of Human Papillomavirus Insertions in Anal Squamous Cell Carcinomas." Cancers 11, no. 12 (November 22, 2019): 1846. http://dx.doi.org/10.3390/cancers11121846.

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The role of human papillomavirus (HPV) in anal squamous cell carcinoma (ASCC) carcinogenesis has been clearly established, involving the expression of viral oncoproteins and optional viral DNA integration into the host genome. In this article, we describe the various mechanisms and sites of HPV DNA insertion and assess their prognostic and predictive value in a large series of patients with HPV-positive ASCC with long-term follow-up. We retrospectively analyzed 96 tumor samples from 93 HPV-positive ASCC patients using the Capture-HPV method followed by Next-Generation Sequencing, allowing determination of HPV genotype and identification of the mechanisms and sites of viral genome integration. We identified five different mechanistic signatures of HPV insertions. The distribution of HPV signatures differed from that previously described in HPV-positive cervical carcinoma (p < 0.001). In ASCC samples, the HPV genome more frequently remained in episomal form (45.2%). The most common signature of HPV insertion was MJ-SC (26.9%), i.e., HPV–chromosomal junctions scattered at different loci. Functionally, HPV integration signatures were not associated with survival or response to treatment, but were associated with viral load (p = 0.022) and PIK3CA mutation (p = 0.0069). High viral load was associated with longer survival in both univariate (p = 0.044) and multivariate (p = 0.011) analyses. Finally, HPV integration occurred on most human chromosomes, but intragenic integration into the NFIX gene was recurrently observed (n = 4/51 tumors). Overall, the distribution of mechanistic signatures of HPV insertions in ASCC was different from that observed in cervical carcinoma and was associated with viral load and PIK3CA mutation. We confirmed recurrent targeting of NFIX by HPV integration, suggesting a role for this gene in ASCC carcinogenesis.

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42

Takeda, Haruhiko, Atsushi Takai, Eriko Iguchi, Masako Mishima, Soichi Arasawa, Ken Kumagai, Yuji Eso, et al. "Oncogenic transcriptomic profile is sustained in the liver after the eradication of the hepatitis C virus." Carcinogenesis 42, no. 5 (February 22, 2021): 672–84. http://dx.doi.org/10.1093/carcin/bgab014.

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Abstract Hepatocellular carcinoma (HCC) developing after hepatitis C virus (HCV) eradication is a serious clinical concern. However, molecular basis for the hepatocarcinogenesis after sustained virologic response (SVR) remains unclear. In this study, we aimed to unveil the transcriptomic profile of post-SVR liver tissues and explore the molecules associated with post-SVR carcinogenesis. We analysed 90 RNA sequencing datasets, consisting of non-cancerous liver tissues including 20 post-SVR, 40 HCV-positive and 7 normal livers, along with Huh7 cell line specimens before and after HCV infection and eradication. Comparative analysis demonstrated that cell cycle- and mitochondrial function-associated pathways were altered only in HCV-positive non-cancerous liver tissues, whereas some cancer-related pathways were up-regulated in the non-cancerous liver tissues of both post-SVR and HCV-positive cases. The persistent up-regulation of carcinogenesis-associated gene clusters after viral clearance was reconfirmed through in vitro experiments, of which, CYR61, associated with liver fibrosis and carcinogenesis in several cancer types, was the top enriched gene and co-expressed with cell proliferation-associated gene modules. To evaluate whether this molecule could be a predictor of hepatocarcinogenesis after cure of HCV infection, we also examined 127 sera from independent HCV-positive cohorts treated with direct-acting antivirals (DAAs), including 60 post-SVR-HCC patients, and found that the elevated serum Cyr61 was significantly associated with early carcinogenesis after receiving DAA therapy. In conclusion, some oncogenic transcriptomic profiles are sustained in liver tissues after HCV eradication, which might be a molecular basis for the liver cancer development even after viral clearance. Among them, up-regulated CYR61 could be a possible biomarker for post-SVR-HCC.

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Haręża, Daria A., Jacek R. Wilczyński, and Edyta Paradowska. "Human Papillomaviruses as Infectious Agents in Gynecological Cancers. Oncogenic Properties of Viral Proteins." International Journal of Molecular Sciences 23, no. 3 (February 5, 2022): 1818. http://dx.doi.org/10.3390/ijms23031818.

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Human papillomaviruses (HPVs), which belong to the Papillomaviridae family, constitute a group of small nonenveloped double-stranded DNA viruses. HPV has a small genome that only encodes a few proteins, and it is also responsible for 5% of all human cancers, including cervical, vaginal, vulvar, penile, anal, and oropharyngeal cancers. HPV types may be classified as high- and low-risk genotypes (HR-HPVs and LR-HPVs, respectively) according to their oncogenic potential. HR-HPV 16 and 18 are the most common types worldwide and are the primary types that are responsible for most HPV-related cancers. The activity of the viral E6 and E7 oncoproteins, which interfere with critical cell cycle points such as suppressive tumor protein p53 (p53) and retinoblastoma protein (pRB), is the major contributor to HPV-induced neoplastic initiation and progression of carcinogenesis. In addition, the E5 protein might also play a significant role in tumorigenesis. The role of HPV in the pathogenesis of gynecological cancers is still not fully understood, which indicates a wide spectrum of potential research areas. This review focuses on HPV biology, the distribution of HPVs in gynecological cancers, the properties of viral oncoproteins, and the molecular mechanisms of carcinogenesis.

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Shah, Rameez, Debesh Chandra Talukdar, Md Abu Yousuf Fakir, AF Mohiuddin Khan, Raj Datta, and Tazin Afrose Shah. "Oral Carcinogenesis and role of Bacteria." Journal of Dhaka Medical College 22, no. 2 (January 9, 2015): 211–15. http://dx.doi.org/10.3329/jdmc.v22i2.21545.

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Cancer, till date stands rigidly unconquered despite most strenuous effort and relentless endeavor by the scientists around the world. In global terms Oral cancer is among the most common malignancy and represents one of the greatest management challenges for the otolaryngologists as well as by the head and neck surgical oncologists. Besides accumulation of genetic mutations, numerous other carcinogens including viral and chemical are well studied and documented. However, in the oral cavity, the role of microbiota in carcinogenesis is not known. Microbial populations on mouth mucosa differ between healthy and malignant sites, and certain oral bacterial species have been linked with malignancies, but the evidence is still weak in this respect. Nevertheless, oral microorganisms inevitably upregulate cytokines and other inflammatory mediators that affect the complex metabolic pathways, and may thus be involved in carcinogenesis. Poor oral health also associates statistically with prevalence of many types of cancer such as pancreatic and gastrointestinal cancer. This review presents commonly implicated bacteria in oral carcinogenesis, and their role in cancer therapeutics as well. DOI: http://dx.doi.org/10.3329/jdmc.v22i2.21545 J Dhaka Medical College, Vol. 22, No.2, October, 2013, Page 211-215

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Gałązka, Jakub Krzysztof, Piotr Homa, and Łukasz Domagalski. "endocrine background of meningioma carcinogenesis." Journal of Education, Health and Sport 13, no. 2 (December 29, 2022): 196–200. http://dx.doi.org/10.12775/jehs.2023.13.02.028.

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Meningiomas, being mostly benign tumors, are derived from the arachnoid cap cells, their etiopathogenesis is based on various factors. The etiology of sporadic meningiomas is not yet known. Many factors have been identified as possible causes of the development of intracranial meningiomas. These include head trauma, viral infections, deletion in the NF2 gene, the use of cell phones, and sex hormones. The review is based on a endocrine factors, playing a role in meningioma carcinogenesis. The carcinogenesis of meningioma appeals to be profoundly dependent from hormonal factors. Mayor ones, usually underlined in according to their prognostic significance, are female sex hormones. Due to this, meningiomas are twice as more likely to occur in female than in male patients. The other group of hormones appointed to play a role in meningioma carcinogenesis are adipokines in general – and leptin in particular. Leptin secretion correlates with BMI elevation, what may explain the confirmed linking between obesity and brain tumors. The scientific literature has documented the occurrence of meningioma in five patients with CAH, but the role of cortical axis and/or ACTH secretion impairments is still under consideration. Authors didn’t find any publication about the role of thyroid disorders in meningioma carcinogenesis. The carcinogenesis of meningioma appeals to be profoundly dependent from hormonal factors. The effects of female sex hormones and adipokines are under a significant consideration, and may be useful in severity prediction. Basic science research should be focused on ACTH secretion in meningioma and possible common genetic etiopathogenesis of meningioma and CAH.

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Smith, Nicola J., and Tim R. Fenton. "The APOBEC3 genes and their role in cancer: insights from human papillomavirus." Journal of Molecular Endocrinology 62, no. 4 (May 2019): R269—R287. http://dx.doi.org/10.1530/jme-19-0011.

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The interaction between human papillomaviruses (HPV) and the apolipoprotein-B mRNA-editing catalytic polypeptide-like (APOBEC)3 (A3) genes has garnered increasing attention in recent years, with considerable efforts focused on understanding their apparent roles in both viral editing and in HPV-driven carcinogenesis. Here, we review these developments and highlight several outstanding questions in the field. We consider whether editing of the virus and mutagenesis of the host are linked or whether both are essentially separate events, coincidentally mediated by a common or distinct A3 enzymes. We discuss the viral mechanisms and cellular signalling pathways implicated in A3 induction in virally infected cells and examine which of the A3 enzymes might play the major role in HPV-associated carcinogenesis and in the development of therapeutic resistance. We consider the parallels between A3 induction in HPV-infected cells and what might be causing aberrant A3 activity in HPV-independent cancers such as those arising in the bladder, lung and breast. Finally, we discuss the implications of ongoing A3 activity in tumours under treatment and the therapeutic opportunities that this may present.

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Munger, Karl, and D. Leanne Jones. "Human Papillomavirus Carcinogenesis: an Identity Crisis in the Retinoblastoma Tumor Suppressor Pathway." Journal of Virology 89, no. 9 (February 11, 2015): 4708–11. http://dx.doi.org/10.1128/jvi.03486-14.

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Viruses are obligate intracellular parasites and need to reprogram host cells to establish long-term persistent infection and/or to produce viral progeny. Cellular changes initiated by the virus trigger cellular defense responses to cripple viral replication, and viruses have evolved countermeasures to neutralize them. Established models have suggested that human papillomaviruses target the retinoblastoma (RB1) and TP53 tumor suppressor networks to usurp cellular replication, which drives carcinogenesis. More recent studies, however, suggest that modulating the activity of the Polycomb family of transcriptional repressors and the resulting changes in epigenetic regulation are proximal steps in the rewiring of cellular signaling circuits. Consequently, RB1 inactivation evolved to tolerate the resulting cellular alterations. Therefore, epigenetic reprograming results in cellular “addictions” to pathways for survival. Inhibition of such a pathway could cause “synthetic lethality” in adapted cells while not markedly affecting normal cells and could prove to be an effective therapeutic approach.

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Kaźmierczak-Siedlecka, Karolina, Agnieszka Daca, Giandomenico Roviello, Martina Catalano, and Karol Połom. "Interdisciplinary insights into the link between gut microbiome and gastric carcinogenesis—what is currently known?" Gastric Cancer 25, no. 1 (November 6, 2021): 1–10. http://dx.doi.org/10.1007/s10120-021-01260-y.

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AbstractCurrently, gastric cancer is one of the leading death-related cancer globally. The etiopathogenesis of gastric cancer is multifactorial and includes among others dysbiotic alterations of gastric microbiota. Molecular techniques revealed that stomach is not a sterile organ and it is resides with ecosystem of microbes. Due to the fact that the role of Helicobacter pylori infection in development of gastric cancer is established and well-studied, this paper is mainly focused on the role of other bacterial as well as viral and fungal gut microbiota imbalance in gastric carcinogenesis. Notably, not only the composition of gastric microbiota may play an important role in development of gastric cancer, but also its activity. Microbial metabolites, such as short-chain fatty acids, polyamines, N-nitroso compounds, and lactate, may significantly affect gastric carcinogenesis. Therefore, this paper discussed aforementioned aspects with the interdisciplinary insights (regarding also immunological point of view) into the association between gut microbiome and gastric carcinogenesis based on up-to-date studies.

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Viarisio, Daniele, Karin Müller Decker, Birgit Aengeneyndt, Christa Flechtenmacher, Lutz Gissmann, and Massimo Tommasino. "Human papillomavirus type 38 E6 and E7 act as tumour promoters during chemically induced skin carcinogenesis." Journal of General Virology 94, no. 4 (April 1, 2013): 749–52. http://dx.doi.org/10.1099/vir.0.048991-0.

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Many findings support a possible involvement of a subgroup of human papillomaviruses (HPVs), called cutaneous beta HPV types, in the development of non-melanoma skin cancer. The skin of transgenic (Tg) mice expressing viral oncoproteins E6 and E7 from different cutaneous beta HPV types, including HPV38, showed an increased susceptibility to UV-induced and/or chemically induced skin carcinogenesis compared with wild-type animals. In this study, we show that beta HPV38 E6 and E7 oncoproteins act as promoter and progression factors in multi-stage skin carcinogenesis, strongly cooperating with the initiator and DNA damage agent 7,12-dimethylbenz[a]anthracene. In contrast, exposure of HPV38 E6/E7 Tg mice to the promoter 12-O-tetradecanoylphorbol-13-acetate did not significantly result in the development of skin lesions. These findings further support the role of beta HPV types in skin carcinogenesis, providing additional insight into their precise contribution to the multi-step process.

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Ikejima, Kenichi, Kazuyoshi Kon, and Shunhei Yamashina. "Nonalcoholic fatty liver disease and alcohol-related liver disease: From clinical aspects to pathophysiological insights." Clinical and Molecular Hepatology 26, no. 4 (October 1, 2020): 728–35. http://dx.doi.org/10.3350/cmh.2020.0202.

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Two major causes of steatohepatitis are alcohol and metabolic syndrome. Although the underlying causes of alcoholrelated liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH) differ, there are certain similarities in terms of the mode of disease progression and underlying pathophysiological mechanisms. Further, excessive alcohol consumption is often seen in patients with metabolic syndrome, and alcoholic hepatitis exacerbation by comorbidity with metabolic syndrome is an emerging clinical problem. There are certain ethnic differences in the development of both NAFLD and ALD. Especially, Asian populations tend to be more susceptible to NAFLD, and genetic polymorphisms in patatin-like phospholipase domain-containing 3 (PNPLA3) play a key role in both NAFLD and ALD. From the viewpoint of pathophysiology, cellular stress responses, including autophagy and endoplasmic reticulum (ER) stress, are involved in the development of cellular injury in steatohepatitis. Further, gutderived bacterial products and innate immune responses in the liver most likely play a profound role in the pathogenesis of both ALD and NASH. Though the recent progress in the treatment of viral hepatitis has reduced the prevalence of viral-related development of hepatocellular carcinoma (HCC), non-viral HCC is increasing. Alcohol and metabolic syndrome synergistically exacerbate progression of steatohepatitis, resulting in carcinogenesis. The gut-liver axis is a potential therapeutic and prophylactic target for steatohepatitis and subsequent carcinogenesis.

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