-
Seminars in Cancer Biology Nov 2022Despite decades of research, cancer continues to be a major global health concern. In recent years, the role played by microorganisms in the development and progression... (Review)
Review
Despite decades of research, cancer continues to be a major global health concern. In recent years, the role played by microorganisms in the development and progression of cancer has come under increased scrutiny. The aim of the present review is to highlight the main associations between members of the human oral microbiota and various cancers. The PubMed database was searched for available literature to outline the current state of understanding regarding the role of the oral microbiota and a variety of human cancers. Oral squamous cell carcinoma (OSCC) is associated with carriage of a number of oral bacteria (e.g., Porphyromonas gingivalis, Fusobacterium nucleatum, Streptococcus sp.), certain viruses (e.g., human papilloma virus, human herpes virus 8, herpes simplex virus 1 and Epstein-Barr virus) and yeast (Candida albicans). Moreover, members of the oral microbiota are associated with cancers of the esophagus, stomach, pancreas, colon/rectum and lung. Furthermore, the present review outlines a number of the carcinogenic mechanisms underlying the presented microbial associations with cancer. Such information may one day help clinicians to diagnose neoplastic diseases at earlier stages and prescribe treatments that take into account the possible microbial nature of carcinogenesis.
Topics: Humans; Mouth Neoplasms; Carcinoma, Squamous Cell; Epstein-Barr Virus Infections; Herpesvirus 4, Human; Microbiota; Carcinogenesis; Head and Neck Neoplasms
PubMed: 34743032
DOI: 10.1016/j.semcancer.2021.11.002 -
Viruses Feb 2023Epstein-Barr virus (EBV) is an oncogenic virus infecting more than 95% of the world's population. After primary infection-responsible for infectious mononucleosis in... (Review)
Review
Epstein-Barr virus (EBV) is an oncogenic virus infecting more than 95% of the world's population. After primary infection-responsible for infectious mononucleosis in young adults-the virus persists lifelong in the infected host, especially in memory B cells. Viral persistence is usually without clinical consequences, although it can lead to EBV-associated cancers such as lymphoma or carcinoma. Recent reports also suggest a link between EBV infection and multiple sclerosis. In the absence of vaccines, research efforts have focused on virological markers applicable in clinical practice for the management of patients with EBV-associated diseases. Nasopharyngeal carcinoma is an EBV-associated malignancy for which serological and molecular markers are widely used in clinical practice. Measuring blood EBV DNA load is additionally, useful for preventing lymphoproliferative disorders in transplant patients, with this marker also being explored in various other EBV-associated lymphomas. New technologies based on next-generation sequencing offer the opportunity to explore other biomarkers such as the EBV DNA methylome, strain diversity, or viral miRNA. Here, we review the clinical utility of different virological markers in EBV-associated diseases. Indeed, evaluating existing or new markers in EBV-associated malignancies or immune-mediated inflammatory diseases triggered by EBV infection continues to be a challenge.
Topics: Humans; Epstein-Barr Virus Infections; Herpesvirus 4, Human; Lymphoma; Lymphoproliferative Disorders; Nasopharyngeal Neoplasms
PubMed: 36992365
DOI: 10.3390/v15030656 -
Recent Results in Cancer Research.... 2021Approximately, 1.4 million virus-induced cancers occur annually, representing roughly 10% of the worldwide cancer burden, with the majority (> 85%) occurring in the...
Approximately, 1.4 million virus-induced cancers occur annually, representing roughly 10% of the worldwide cancer burden, with the majority (> 85%) occurring in the lower- and middle-income countries. The viruses associated with the greatest number of cancer cases are human papillomaviruses (HPVs), which cause cervical cancer and several other epithelial malignancies, and hepatitis viruses HBV and HCV, which are responsible for the majority of hepatocellular cancer. Other oncoviruses include Epstein-Barr virus (EBV), Kaposi's sarcoma herpesvirus (KSHV), human T-cell leukemia virus (HTLV-I), and Merkel cell polyoma virus (MCPyV). These oncoviruses include various classes of DNA and RNA viruses and induce cancer by a variety of mechanisms. However, cancers develop in a minority of infected individuals and almost always after chronic infection of many year's duration. Identification of the oncoviruses has provided critical insights in human carcinogenesis and led to several interventions that may reduce the risk of developing the tumors they induce. These interventions include preventive vaccines against HBV and HPV, screening for persistent HPV and HCV infections, antivirals for the treatment of chronic HBV and HCV infection, and screening the blood supply for the presence of HBV and HCV. Further efforts to identify additional oncogenic viruses in human cancers and new insights into etiology and pathogenesis of virally induced cancers would likely lead to new approaches for prophylactic and therapeutic interventions.
Topics: Carcinogenesis; Carcinoma, Hepatocellular; Herpesvirus 4, Human; Humans; Neoplasms; Oncogenic Viruses; Virus Diseases
PubMed: 33200359
DOI: 10.1007/978-3-030-57362-1_1 -
Nature Reviews. Microbiology Nov 2018Viral infection is a major contributor to the global cancer burden. Recent advances have revealed that seven known oncogenic viruses promote tumorigenesis through shared... (Review)
Review
Viral infection is a major contributor to the global cancer burden. Recent advances have revealed that seven known oncogenic viruses promote tumorigenesis through shared host cell targets and pathways. A comprehensive understanding of the principles of viral oncogenesis may enable the identification of unknown infectious aetiologies of cancer and the development of therapeutic or preventive strategies for virus-associated cancers. In this Review, we discuss the molecular mechanisms of viral oncogenesis in humans. We highlight recent advances in understanding how viral manipulation of host cellular signalling, DNA damage responses, immunity and microRNA targets promotes the initiation and development of cancer.
Topics: Carcinogenesis; DNA Damage; Host-Pathogen Interactions; Humans; Immunity; MicroRNAs; Neoplasms; Oncogenic Viruses; Signal Transduction; Tumor Virus Infections
PubMed: 30143749
DOI: 10.1038/s41579-018-0064-6 -
Virologica Sinica Apr 2015
Topics: Host-Pathogen Interactions; Humans; Neoplasms; Oncogenic Viruses
PubMed: 25924992
DOI: 10.1007/s12250-015-3599-y -
Emerging Infectious Diseases May 2014
Topics: Cell Transformation, Viral; History, 20th Century; Humans; Oncogenic Viruses; Research
PubMed: 24751102
DOI: 10.3201/eid2005.131876 -
Philosophical Transactions of the Royal... Oct 2017A viral etiology of cancer was first demonstrated in 1911 by Peyton Rous who injected cell-free filtrate from a chicken sarcoma into healthy chickens and found it... (Review)
Review
A viral etiology of cancer was first demonstrated in 1911 by Peyton Rous who injected cell-free filtrate from a chicken sarcoma into healthy chickens and found it induced a tumour. Since the discovery over 50 years ago of the Epstein-Barr virus as the cause of Burkitt lymphoma, seven other human viruses or groups of viruses-hepatitis B virus, hepatitis C virus, human immunodeficiency virus type 1, some human papillomaviruses, human T-cell lymphotropic virus type 1, Kaposi sarcoma-associated herpesvirus and Merkel cell polyomavirus-have been linked to human cancer. Collectively, these eight viruses cause over 20 different types of cancer and contribute to 10-12% of all cancer, with a greater burden in low- and middle-income countries. For many viruses, immunosuppression greatly increases the risks of persistent infection, development of chronic sequelae and cancer. Although several viruses share similar routes of transmission (especially sexual activity, injection drug use and mother-to-child transmission), the predominant route of transmission varies across viruses, and for the same virus can vary by geographical location. In general, vulnerable populations at the greatest risk for viral infections and their associated diseases include people, especially children, living in low- to middle-income countries, men who have sex with men, people who use injection drugs and female sex workers.This article is part of the themed issue 'Human oncogenic viruses'.
Topics: Humans; Oncogenic Viruses; Tumor Virus Infections
PubMed: 28893933
DOI: 10.1098/rstb.2016.0266 -
Philosophical Transactions of the Royal... Apr 2001The persisting ancient view of cancer as a contagious disease ended with 19th century scientific investigations which seemed to show it was not. The resulting dogma... (Review)
Review
The persisting ancient view of cancer as a contagious disease ended with 19th century scientific investigations which seemed to show it was not. The resulting dogma against an infectious cause for cancer produced great prejudice in the scientific community against the first report of an oncogenic virus by Rous early in the 20th century and, even in the 1950s, against Gross's finding of a murine leukaemia virus and a murine virus causing solid tumours. The Lucké frog renal carcinoma virus was the first cancer-associated herpesvirus. Intriguingly, an environmental factor, ambient temperature, determines virus genome expression in the poikilothermic frog cells. Although an alpha-herpesvirus, Marek's disease virus of chickens shares some aspects of biological behaviour with Epstein-Barr virus (EBV) of man. Very significantly, its lymphomas are the first naturally occurring malignancy to be controlled by an antiviral vaccine, with implications for human virus-associated cancers. The circumstances and climate of opinion in which successive gamma-herpesviruses were discovered are described. The identification of EBV involved two unconventionalities: its finding in cultured Burkitt's lymphoma cells when no human lymphoid cell had ever been maintained in vitro, and its recognition in the absence of biological activity by the then new technique of electron microscopy. These factors engendered hostility to its acceptance as a new human tumour-associated virus. The EBV-like agents of Old World apes and monkeys and the T-lymphotropic gamma-herpesviruses of New World monkeys were found at about the same time, not long after the discovery of EBV. For many years these were thought to be the only gamma-herpesviruses of non-human primates; however, very recently B-lymphotropic EBV-like agents have been identified in New World species as well. Mouse herpesvirus 68 came to light by chance during a search for arboviruses and has become important as a laboratory model because of its close genetic relatedness to EBV and its comparable biological behaviour. The discovery of Kaposi's sarcoma-associated herpesvirus six years ago was made using unconventional new methods, but, unlike with EBV 30 years before, this did not hinder its acceptance. This contrast is discussed in the context of the great progress in human tumour virology which has been made in recent years.
Topics: Animals; Birds; Herpesvirus 2, Gallid; History, 20th Century; Humans; Neoplasms; Oncogenic Viruses; Tumor Virus Infections; Viral Vaccines; Virology
PubMed: 11313002
DOI: 10.1098/rstb.2000.0774 -
Oxidative Medicine and Cellular... 2017Approximately 20% of human cancers is attributable to DNA oncogenic viruses such as human papillomavirus (HPV), hepatitis B virus (HBV), and Epstein-Barr virus (EBV).... (Review)
Review
Approximately 20% of human cancers is attributable to DNA oncogenic viruses such as human papillomavirus (HPV), hepatitis B virus (HBV), and Epstein-Barr virus (EBV). Unrepaired DNA damage is the most common and overlapping feature of these DNA oncogenic viruses and a source of genomic instability and tumour development. Sustained DNA damage results from unceasing production of reactive oxygen species and activation of inflammasome cascades that trigger genomic changes and increased propensity of epigenetic alterations. Accumulation of epigenetic alterations may interfere with genome-wide cellular signalling machineries and promote malignant transformation leading to cancer development. Untangling and understanding the underlying mechanisms that promote these detrimental effects remain the major objectives for ongoing research and hope for effective virus-induced cancer therapy. Here, we review current literature with an emphasis on how DNA damage influences HPV, HVB, and EBV replication and epigenetic alterations that are associated with carcinogenesis.
Topics: DNA Tumor Viruses; Epigenesis, Genetic; Genomics; Humans; Oxidative Stress
PubMed: 28740569
DOI: 10.1155/2017/3179421 -
Viruses Jul 2020Basic leucine zipper (bZIP) transcription factors (TFs) govern diverse cellular processes and cell fate decisions. The hallmark of the leucine zipper domain is the... (Review)
Review
Basic leucine zipper (bZIP) transcription factors (TFs) govern diverse cellular processes and cell fate decisions. The hallmark of the leucine zipper domain is the heptad repeat, with leucine residues at every seventh position in the domain. These leucine residues enable homo- and heterodimerization between ZIP domain α-helices, generating coiled-coil structures that stabilize interactions between adjacent DNA-binding domains and target DNA substrates. Several cancer-causing viruses encode viral bZIP TFs, including human T-cell leukemia virus (HTLV), hepatitis C virus (HCV) and the herpesviruses Marek's disease virus (MDV), Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV). Here, we provide a comprehensive review of these viral bZIP TFs and their impact on viral replication, host cell responses and cell fate.
Topics: Animals; Basic-Leucine Zipper Transcription Factors; Deltaretrovirus; Herpesvirus 4, Human; Herpesvirus 8, Human; Humans; Mardivirus; Oncogenic Viruses; Phylogeny; Tumor Virus Infections; Unfolded Protein Response
PubMed: 32674309
DOI: 10.3390/v12070757