Relevant bibliographies by topics / Viral carcinogenesis

Academic literature on the topic 'Viral carcinogenesis'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Viral carcinogenesis.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Viral carcinogenesis"

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
Abstract:
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
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Viral carcinogenesis"

1

CORTESE, MARIA FRANCESCA. "HIV and HBV infection as models of viral DNA integration and mechanisms of viral-associated carcinogenesis." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2015. http://hdl.handle.net/2108/203036.

Full text
Abstract:
My PhD was focused on two viruses, both responsible of persistent infection: HIV and HBV. The two viruses show high worldwide prevalence and both are associated with high morbidity and mortality. HIV establishes a persistent infection through different mechanisms, first of all with the integration of its DNA into the host genome, thus forming the provirus. However, a consistent part of the viral DNA within the infected cells is unintegrated (circular or not). The project following presented aims to analyse the kinetic of viral replication (measured as p24 production) and HIV DNA integration in primary lymphocytes (CD4+ ad PBMC) and Monocyte-derived Macrophages (MdM) in presence and absence of Integrase inhibitors (INIs). HIV DNA quantification (as proviral, unintegrated and 2-LTR) was assessed at different time points. The presented data reconfirmed, as previously reported in literature, the different kinetic of HIV replication in lymphocytes (CD4+ T cells and PBMCs, much faster) compared to macrophages (more slow), and suggested the presence of a different kinetic of HIV DNA integration between the two cellular systems, too. Both INIs efficiently inhibit the viral replication and the integration of HIV DNA. However, a little but consistent amount of HIV DNA was observed at 30 days post treatment in macrophages, which are the main reservoirs of the infection. By analysing the composition of this little HIV DNA amount, we observed a very little difference between the two drug which could be probably explained by the well-described different kinetic of dissociation of the DTG-enzyme complex. In conclusion these data could give new information about the different kinetic of HIV replication between lymphocytes and macrophages, suggesting also the implication of a different kinetic of HIV DNA integration. Both the integrase inhibitors efficiently inhibit HIV replication and integration. Nonetheless, in presence of INI, although an almost total inhibition of HIV replication was observed, a little but consistent amount of viral DNA was maintained in macrophages. This evidence could have important implication in the study of HIV persistence and viral rebound after treatment interruption. The data above mentioned were presented at the 12th edition of the European congress on HIV e hepatitis, in Barcelona in 2014 (26-28 March), and a manuscript is in preparation. HBV is another important virus able to establish a persistent infection that usually causes cirrhosis and hepatocarcinoma (HCC). HBV could indirectly (through compensative cellular replication) or directly (through event of random integration or due to the viral proteins) promote carcinogenesis. Among the viral proteins the trans-activating HBV protein (HBx) covers a key role in this sense. The project here presented aims to highlight specific mutations in HBX gene associated with HCC in a group of chronically-HBV infected patients. By analysing the sequences of 75 HBV chronically infected patients, we observed the mutation F30V prevalently in the HCC group. This is located within the N-terminal region of HBx which seems to be involved in the negative regulation of the HBx trans-activation function. By analysing the results obtained in vitro, we observed that the mutation would reduce the viral replication, probably due to its localization in a domain within the N-terminal region known to be involve in the dimerization of the protein. HBx protein, both wt and mutated, did not alter the cycle progression of exposed cells. On the contrary, the mutation could to be associated with less cellular susceptibility to apoptotic death related to what observed in presence of the HBx wt. This observed cell survival could probably promote the maintenance of aberrant cellular clones thus favouring the appearance of tumour. Of consequence, considering the obtained results, it is possible to propose that F30V mutation could interfere with HBV replication and can have a role in HBV-driven carcinogenesis by reducing the rate of apoptosis. However, further studies are required in order to understand the potential role of F30V as HCC prognostic factor in HBV chronically infected patients.
APA, Harvard, Vancouver, ISO, and other styles
2

Siouda, Maha. "Transcriptional regulation and epigenetic repression of the tumor suppressor DOK1 in viral- and non viral-related carcinogenesis." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10163.

Full text
Abstract:
Le suppresseur de tumeur DOK1 (downstream of tyrosine kinases1) est une protéine régulatrice de voies de signalisation impliquées dans des processus cellulaires tel que la prolifération, la migration et l'apoptose. Le rôle suppresseur de tumeur de DOK1 a été démontré dans des modèles animaux. Les souris knock-out pour DOK1 présentent une forte susceptibilité de développer des leucémies, des tumeurs malignes hématologiques, des adénocarcinomes pulmonaires, ainsi que des sarcomes histiocytaires agressifs. En outre, nous avons rapporté précédemment que le gène DOK1 peut être muté et son expression réprimée dans différentes tumeurs malignes humaines, telles que les lignées cellulaires de lymphome de Burkitt (BL) et la leucémie lymphoïde chronique (LLC). Cependant, les mécanismes de dérégulation de DOK1 restent inconnus, notamment dans les processus de carcinogenèse induite ou non par des oncovirus. Dans ce projet de thèse, nous avons d'abord caractérisé le promoteur de DOK1 et le rôle du facteur de transcription E2F1 comme le principal régulateur de l'expression de DOK1. Nous avons démontré pour la première fois la contribution de DOK1 dans la réponse cellulaire au stress par son rôle suppresseur de prolifération cellulaire et promoteur d'apoptose. Nous avons trouvé que l'expression du gène DOK1 est réprimée dans une variété de cancers humains, y compris le cancer de la tête et du cou, les lymphomes de Burkitt et les cancers du poumon. Cette répression est due à l'hyperméthylation aberrante de DOK1. Nous avons donc étudié les événements épigénétiques, qui sont souvent altérés dans les cancers, et leurs implications dans la répression de DOK1 dans les lignes cellulaire cancéreuses de la tête et du cou. Nous nous sommes par la suite intéressés aux mécanismes de dérégulation de DOK1 par le virus d'Epstein Barr dans le cadre de sa propriété oncogénique dans les lymphocytes B humains ainsi que dans les lignes cancéreuses du lymphome de Burkitt. Nos résultats apportent de nouvelles informations sur les mécanismes de régulation de l'expression de DOK1 dans la carcinogenèse induite ou non par des oncovirus, ce qui pourrait le définir comme un biomarqueur potentiel de cancer et comme une cible intéressante pour des thérapies épigénétiques
The newly identified tumor suppressor DOK1 (downstream of tyrosine kinases1) inhibits cell proliferation, negatively regulates MAP kinase activity, opposes leukemogenesis, and promotes cell spreading, motility, and apoptosis. DOK1 also plays a role in the regulation of immune cell activation, including B cells. The tumor suppressor role of DOK1 was demonstrated in animal models. DOK1 knockout mice show a high susceptibility to develop leukemia, hematological malignancies as well as lung adenocarcinomas and aggressive histiocytic sarcoma. In addition, we previously reported that the DOK1 gene can be mutated and its expression is down-regulated in human malignancies such as Burkitt’s lymphoma cell lines (BL) and chronic lymphocytic leukemia (CLL). However, very little is known about the mechanisms underlying DOK1 gene regulation and silencing in viral- and non viral-related tumorigenesis. In the present project, we first characterized the DOK1 promoter. We have shown the role of E2F1 transcription factor as the major regulator of DOK1 expression and how DOK1 plays a role in DNA stress response though opposing cell proliferation and promoting apoptosis. We demonstrated that DOK1 gene expression is repressed in a variety of human cancers, including head and neck, Burkitt’s lymphoma and lung cancers, as a result of aberrant hypermethylation. We investigated the link between the epigenetic events and DOK1 silencing in non viral head and neck cancer cell lines, and by Epstein Barr virus in relation to its oncogenic activity in human B cells and neoplasia such as Burkitt’s lymphoma. These data provide novel insights into the regulation of DOK1 in viral and non viral-related carcinogenesis, and could define it as a potential cancer biomarker and an attractive target for epigeneticbased therapy
APA, Harvard, Vancouver, ISO, and other styles
3

Tiniakos, Konstantina G. "Production, characterisation and clinical application of monoclonal antibodies to the human c-jun and c-fos oncoproteins." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246089.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Pierce, Angela Marie. "Deregulated E2F1 has both oncogenic and tumor suppressive properties in mouse skin /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Wang, Ling, Guang Y. Li, Jonathan P. Moorman, and Shunbin Ning. "MicroRNA Regulation Of Viral Immunity, Latency, And Carcinogenesis of Selected Tumor Viruses and HIV." Digital Commons @ East Tennessee State University, 2015. https://doi.org/10.1002/rmv.1850.

Full text
Abstract:
MicroRNAs (miRNAs) function as key regulators in immune responses and cancer development. In the contexts of infection with oncogenic viruses, miRNAs are engaged in viral persistence, latency establishment and maintenance, and oncogenesis. In this review, we summarize the potential roles and mechanisms of viral and cellular miRNAs in the host-pathogen interactions during infection with selected tumor viruses and HIV, which include (i) repressing viral replication and facilitating latency establishment by targeting viral transcripts, (ii) evading innate and adaptive immune responses via toll-like receptors, RIG-I-like receptors, T-cell receptor, and B-cell receptor pathways by targeting signaling molecules such as TRAF6, IRAK1, IKKε, and MyD88, as well as downstream targets including regulatory cytokines such as tumor necrosis factor α, interferon γ, interleukin 10, and transforming growth factor β, (iii) antagonizing intrinsic and extrinsic apoptosis pathways by targeting pro-apoptotic or anti-apoptotic gene transcripts such as the Bcl-2 family and caspase-3, (iv) modulating cell proliferation and survival through regulation of the Wnt, PI3K/Akt, Erk/MAPK, and Jak/STAT signaling pathways, as well as the signaling pathways triggered by viral oncoproteins such as Epstein-Barr Virus LMP1, by targeting Wnt-inhibiting factor 1, SHIP, pTEN, and SOCSs, and (v) regulating cell cycle progression by targeting cell cycle inhibitors such as p21/WAF1 and p27/KIP1. Further elucidation of the interaction between miRNAs and these key biological events will facilitate our understanding of the pathogenesis of viral latency and oncogenesis and may lead to the identification of miRNAs as novel targets for developing new therapeutic or preventive interventions.
APA, Harvard, Vancouver, ISO, and other styles
6

Ricciardi, Riccardo Pietro 1985. "A role for high-risk HPV type 16 E6 and E7 oncoproteins in colorecteral carcinogenesis /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112351.

Full text
Abstract:
Human papillomavirus (HPV) infections play a crucial role in human carcinogenesis. Greater than 96% of all cervical carcinomas are positive for high-risk HPV infections; especially types 16 and 18. High-risk HPV onco-proteins, E6 and E7, are consistently expressed in such cancers and function by inactivating p53 and pRb tumor suppressors, respectively. The presence of high-risk HPVs is also correlated with anogenital cancers. In this study, we examined the effect of high-risk HPV type 16 E6 and E7 oncoproteins in two normal human colorectal epithelial cell lines, NCE1 and NCE5. We report that the expression of E6/E7 proteins, alone, induced cellular transformation of both cell lines; consequently, NCE1-E6/E7 and NCE5-E6/E7 form colonies in soft agar with respect to their wild type cells. This is accompanied by cell cycle deregulation, as is demonstrated by the over-expression of cyclin dependant kinases (cdks) and their respective cyclins. Furthermore, we demonstrate that E6/E7 oncoprotein transduction induces migration of colorectal epithelial cells. More still, well analyzed Id gene expression, a family member of the helix-loop-helix (HLH) transcription factors involved in the regulation of cell invasion and metastasis of human cancer cells. In parallel, using tissue microarray analysis we found that the four members of the Id protein family are correlated with the presence of HPV type 16 and 18 in human colon cancer tissues. Our data suggests that high-risk HPV infections are sufficient to induce cellular transformation of normal human colorectal cells, in vitro. Furthermore, the correlation with the Id family of proteins may present a novel set of markers associated with HPV induced colorectal carcinogenesis. Our results may suggest a new approach to detect and prevent colorectal cancer.
APA, Harvard, Vancouver, ISO, and other styles
7

Yu, Fang, and 喻芳. "Functional characterization of interferon induced transmembrane protein-1 in colorectal cancer and glioma carcinogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46079956.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Kercher, Lisa A. "Search for the retroviral origin of a novel murine spontaneous lymphoma." Virtual Press, 1994. http://liblink.bsu.edu/uhtbin/catkey/902487.

Full text
Abstract:
It is known that many types of leukemias and lymphomas are of viral origin. A new strain of immunologically deficient mice, the BALB/c x C57B1/6 beige nude mice, has been observed to develop spontaneous lymphomas of unknown origin at a high frequency. It is possible the tumors originate from a retroviral infection, which we attempted to show by detection of viral reverse transcriptase (RT) activity. We measured the (RT) activity in the supernatants of cocultures from the spleen and lymph node tissues of the beige nude animals by two methods, tritiated thymidine triphosphate incorporation in a standard RT assay, and the commercially available RT-DetectTM (DuPont) method. Of all supernatants tested, none showed a significant amount of RT activity compared with a cell line that was known to be actively producing the retrovirus MuLV. Upon electron microscopic analysis of the tumor-like cells grown in coculture, no viral particles were observed. Flow cytometric analysis of the tumor-like cells showed two general phenotypes; one predominately of a helper T cell type, and the other of a less differentiated immature thymocyte type.
Department of Biology
APA, Harvard, Vancouver, ISO, and other styles
9

Amin, Janaki Public Health &amp Community Medicine Faculty of Medicine UNSW. "Hepatitis B and C associated cancer and mortality: New South Wales, 1990-2002." Awarded by:University of New South Wales. School of Public Health and Community Medicine, 2006. http://handle.unsw.edu.au/1959.4/27338.

Full text
Abstract:
This thesis examines cancer and mortality rates among people diagnosed with hepatitis B (HBV) and C (HCV) infection in New South Wales (NSW) from 1990 through 2002, by linking hepatitis notifications with the NSW Central Cancer Registry (CCR) and National Death Index. Of the 39101 HBV, 75834 HCV and 2604 HBV/HCV co-infection notifications included 1052, 1761 and 85 were linked to cancer notifications and 1233, 4008 and 186 were linked to death notifications respectively. Of 2072 hepatocellular carcinoma (HCC) notifications to the CCR 323, 267 and 85 were linked to HBV, HCV and HBV/HCV co-infection notifications. Incidence of HCC was 6.5, 4.0 and 5.9 per 1000 person years for HBV, HCV and HBV/HCV co-infected groups. Risk of HCC in those diagnosed with hepatitis was 20 to 30 times greater than the standard population. There was a marginally statistically significant increased risk of immunoproliferative malignancies associated with HCV infection (SIR=5.6 95% CI 1.8 ???17.5). Risk of death for those with hepatitis was significantly greater, 1.5 to 5 fold, than the general population with the greatest risk among those with HBV/HCV co-infection. The primary cause of HBV deaths was liver related, particularly HCC, whereas in the HCV groups drug related deaths were most frequent. Among people with HCV, risk of dying from drug related causes was significantly greater than from liver related causes (p=0.012), with the greatest increased risk in females age 15- 24 years (SMR 56.9, 95%CI 39.2???79.9). Median age at diagnosis of HCC varied markedly by country of birth and hepatitis group: HBV 66, 63 and 57years ; HCV 51, 68 and 71 years; unlinked 69, 70 and 64 years for Australian, European, and Asian-born groups, respectively (P<0.0001 for all groups). While the risk of cancer, particularly HCC, is elevated among people with HBV and HCV infection, the absolute risk remains low. Young people with HCV face a higher mortality risk from continued drug use than from liver damage related to their HCV infection. The influence of IDU in the epidemiology of HCC in New South Wales was possibly reflected in the varying distributions of age and country of birth.
APA, Harvard, Vancouver, ISO, and other styles
10

Olanrewaju, Folawiyo S., Ayotola Falodun, Muhammed Jawla, Patricia Vanhook, and Stacey McKenzie. "Hepatitis C Virus Screening in Federally Qualified Health Centers in Rural Appalachia." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/90.

Full text
Abstract:
The prevalence of Hepatitis C Virus (HCV) in the US is estimated at 3.5 million with 18,153 deaths in 2016. It is the most common bloodborne infection, with a higher age-adjusted mortality rate than Hepatitis B Virus or Human Immunodeficiency Virus. Without treatment, nearly 1.1 million people will die from HCV by 2060. About 41,200 new cases of HCV were reported in 41 states in the US in 2016. The reported cases of acute HCV in 2016 is 2.3 per 100,000 in Tennessee, which is more than twice the national goal set by Healthy People 2020. This is a descriptive study to ascertain the HCV prevalence and usefulness of screening in medical outreach settings (MO) compared to indigent healthcare clinics (IHC) in northeast Tennessee. This study period was from April 2017 – February 2019. Participants (n=250), were adults, who engaged in routine, opt-out HCV testing at 4 IHC and 3 MO sites in the Tri-Cities, TN region. During the screening, demographic information- age, gender, race- were collected and the de-identified data were analyzed using Statistical Analysis System (SAS 9.3) to perform a descriptive analysis. Also, several discrete Chi-Square tests of independence between the demographic variables, screening locations, and HCV antibody prevalence was conducted. A total of 250 clients were screened for HCV. The majority of clients screened were non-Hispanic whites 228 (91.20%); females 136 (54.40%); young adults 131 (52.40%) and at IHC clinics 187 (74.80%). Screening showed HCV antibody prevalence of 14.8%. The majority of positive cases were non-Hispanic whites 36 (97.30%; P=0.1561); females 19 (51.35%; P=0.6867) and young adults 23 (62.16%; P=0.286). The prevalence at the IHC clinics and MO settings were 36 (97.30%; P=0.0006) and 1(2.70%) respectively. This analysis shows the higher yield of targeted HCV screening at IHC clinics. Focused HCV screening is critical in the era of opioid epidemic, particularly when direct-acting antiviral agents (DAAs) which offer a Sustained Virologic Response (SVR) rate of more than 90% are available. The use of case control or cohort study designs to establish causality is recommended for improving focused HCV screening.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Viral carcinogenesis"

1

Microbes and human carcinogenesis. London: E. Arnold, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Alfred Benzon Symposium. (24th 1986 Copenhagen, Denmark). Viral carcinogenesis: Functional aspects : proceedings of the Alfred Benzon Symposium 24 held at the premises of the Royal Danish Academy of Sciences and Letters, Copenhagen 15-19 June 1986. Copenhagen: Munksgaard, 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Alfred Benzon Symposium (24th 1985 Copenhagen, Denmark). Viral carcinogenesis: Functional aspects : proceedings of the Alfred Benzon Symposium 24 held at the premises of the Royal Danish Academy of Sciences and Letters, Copenhagen 15-19 June 1986. Copenhagen: Munksgaard, 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Rachev, Racho R. Molekuli͡a︡rni mekhanizmi na retrovirusnata i spontannata kant͡s︡erogeneza. Sofii͡a︡: Izd-vo na Bŭlgarskata akademii͡a︡ na naukite, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

1951-, Khalili Kamel, and Jeang Kuan-Teh, eds. Viral oncology: Basic science and clinical applications. Hoboken, N.J: Wiley-Blackwell, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

1951-, Khalili Kamel, and Jeang Kuan-Teh, eds. Viral oncology: Basic science and clinical applications. Hoboken, N.J: Wiley-Blackwell, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

1951-, Khalili Kamel, and Jeang Kuan-Teh, eds. Viral oncology: Basic science and clinical applications. Hoboken, N.J: Wiley-Blackwell, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Das, Dilip K. Viral cancers: Cytologic tools in diagnosis and management. New York: Nova Science, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Das, Dilip K. Viral cancers: Cytologic tools in diagnosis and management. Hauppauge, N.Y: Nova Science, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

1925-, Klein George, ed. Viruses as the causative agents of naturally occurring tumors. New York: Raven Press, 1985.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Viral carcinogenesis"

1

Sarin, Prem S. "Selected Aspects of Viral Carcinogenesis." In Mechanisms of Carcinogenesis, 71–83. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-2526-7_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Lambert, Paul F. "Viral Mechanisms in Human Carcinogenesis." In The Molecular Basis of Human Cancer, 297–306. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-59745-458-2_19.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Hoppe-Seyler, Felix, and Karin Butz. "Viral Mechanisms of Human Carcinogenesis." In The Molecular Basis of Human Cancer, 233–47. Totowa, NJ: Humana Press, 2002. http://dx.doi.org/10.1007/978-1-59259-125-1_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Molho-Pessach, Vered, and Michal Lotem. "Viral Carcinogenesis in Skin Cancer." In Environmental Factors in Skin Diseases, 39–51. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000106409.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

De Mitri, M. S., P. Baccarini, C. Bonazzi, P. Paterlini, and E. Pisi. "Potential Molecular Mechanisms of Viral Liver Carcinogenesis." In New Trends in Hepatology, 183–96. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0357-9_21.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Takada, Shinako, Takeshi Mori, Hiroshi Kido, Ikuo Nakamura, Katsuyuki Yaginuma, Nobuo Tsuchida, and Katsuro Koike. "Contribution of HBV X Gene Expression to Hepatic Carcinogenesis." In Viral Hepatitis and Liver Disease, 753–56. Tokyo: Springer Japan, 1994. http://dx.doi.org/10.1007/978-4-431-68255-4_196.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Ham, A. W., E. A. McCulloch, L. Siminovitch, A. F. Howatson, and A. A. Axelrad. "The Process of Viral Carcinogenesis in the Hamster Kidney with the Polyoma Virus." In Novartis Foundation Symposia, 284–301. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719275.ch14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Smith, A. J., and L. A. Smith. "Viral Carcinogenesis." In Progress in Molecular Biology and Translational Science, 121–68. Elsevier, 2016. http://dx.doi.org/10.1016/bs.pmbts.2016.09.007.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Dittmer, Dirk P., and Blossom Damania. "Viral carcinogenesis." In Oxford Textbook of Cancer Biology, edited by Francesco Pezzella, Mahvash Tavassoli, and David J. Kerr, 71–78. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0006.

Full text
Abstract:
Between 20 and 30% of human cancers are caused by infectious agents. These can be multicellular parasites, bacteria, or viruses. Whereas bacteria and parasites cause cancer by indirect mechanisms, such as inflammation and immune deregulation, viruses infect human cells directly and initiate molecular changes that lead to uncontrolled proliferation. Both DNA and RNA viruses, such as retroviruses, can cause cancer; however, the ability to promote cancer is a by-product of viral evolution and a low frequency event, often the result of faulty virus replication. Most human oncogenes, such as MYC, SRC, RAS, were first discovered because they had been pirated by retroviruses. The function of key human tumour suppressor proteins, such as RB and TP53, were identified because they bind to and are inactivated by DNA tumour viruses. Because viruses are foreign, vaccines can be devised that target them. More recently it has become possible to prevent two types of cancer caused by viruses—cervical cancer caused by human papillomavirus (HPV) and hepatocarcinoma caused by hepatitis B virus (HBV)—by preventing the initial infection using vaccination. Study of the relationship between infective agents and cancer has therefore achieved two main goals: to unravel basic mechanisms of carcinogenesis and to make some cancers preventable.
APA, Harvard, Vancouver, ISO, and other styles
10

Barhoi, Dharmeswar, Sarbani Giri, Puja Upadhaya, and Sweety Nath Barbhuiya. "Chemopreventive and Therapeutic Potential of Phytopharmaceuticals Against Oral Cancer." In Handbook of Research on Advancements in Cancer Therapeutics, 541–69. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-6530-8.ch020.

Full text
Abstract:
Oral cancer is a major public health problem in both developing and developed countries. It is believed to be the eighth most common cancer considering a major risk factor of worldwide morbidity and mortality. Major risk factors of this deadly disease are lifestyle (consumption of smoking and smokeless tobacco, alcohol, betel quid, etc.), unhealthy food, and poor dental care and viral infections. These factors are responsible for mutations in the DNA leading to the initiation of carcinogenesis. Oral carcinogenesis is a multistep process having three distinct phases: initiation, promotion, and progression. Modern cancer treatments (chemotherapy, surgery, radiation therapy, and immunotherapy) are associated with lots of side effects. Thus, phytopharmaceuticals are being used as alternative medicines in the prevention of oral carcinogenesis. Phytopharmaceuticals (such as resveratrol, sulforaphane, quercetin, etc.) have immense potential to prevent cancer development in every phase of carcinogenesis and more importantly, these compounds have fewer side effects.
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Viral carcinogenesis"

1

Speel, Ernst-Jan M., Wendy Theelen, Michael Herfs, Martin Reijans, Guus Simons, Els V. Meulemans, Marcella M. Baldewijns, et al. "Abstract 5368: Increase in viral load, viral integration and gain of telomerase genes during uterine cervical carcinogenesis can be simultaneously assessed by the HPV MLPA-assay." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5368.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Viral carcinogenesis' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography