Both viruses and carcinogenic chemicals can cause tumors by

Matsuoka M, Green PL. Monoclonal integration of human T-cell leukemia provirus in all primary tumors of adult T-cell leukemia suggests causative role of human T-cell leukemia virus in the disease.

Raab-Traub N, Flynn K. The structure of the termini of the Epstein-Barr virus as a marker of clonal cellular proliferation. Russo JJ, et al. Human herpesvirus 8-encoded thymidine kinase and phosphotransferase homologues confer sensitivity to ganciclovir. Martin DF, et al. Oral ganciclovir for patients with cytomegalovirus retinitis treated with a ganciclovir implant.

Little RF, Yarchoan R. Treatment of gammaherpesvirus-related neoplastic disorders in the immunosuppressed host. Mason WS, et al. The amount of hepatocyte turnover that occurred during resolution of transient hepadnavirus infections was lower when virus replication was inhibited with entecavir. Levine AJ. The common mechanisms of transformation by the small DNA tumor viruses: the inactivation of tumor suppressor gene products: p Telomerase activation by human papillomavirus type 16 E6 protein: induction of human telomerase reverse transcriptase expression through Myc and GC-rich Sp1 binding sites.

Telomerase activation by the E6 gene product of human papillomavirus type Kataoka H, et al. Immortalization of immunologically committed Epstein-Barr virus-transformed human B-lymphoblastoid cell lines accompanied by a strong telomerase activity. Terrin L, et al. Mosialos G, et al. The Epstein-Barr virus transforming protein LMP1 engages signaling proteins for the tumor necrosis factor receptor family.

Virus Res. Liu L, et al. Fujimuro M, et al. Antiviral activity of tumor-suppressor pathways: clues from molecular piracy by KSHV. Trends Genet. Human papillomavirus type 16 alters human epithelial cell differentiation in vitro. Munger K, et al. Complex formation of human papillomavirus E7 proteins with the retinoblastoma tumor suppressor gene product. The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p Duensing S, et al.

The human papillomavirus type 16 E6 and E7 oncoproteins cooperate to induce mitotic defects and genomic instability by uncoupling centrosome duplication from the cell division cycle. Hein J, et al. Simian virus 40 large T antigen disrupts genome integrity and activates a DNA damage response via Bub1 binding.

Cancer Biol. Inhibition of p53 tumor suppressor by viral interferon regulatory factor. Gwack Y, et al. Park J, et al.

Virology, pathogenetic mechanisms, and associated diseases of Kaposi sarcoma-associated herpesvirus human herpesvirus 8 Mayo Clin. Pfeffer S, et al. Identification of microRNAs of the herpesvirus family.

Nature Methods. Gottwein E, et al. A viral microRNA functions as an orthologue of cellular miR Choy EY, et al. Epstein-Barr virus: 40 years on. The latent nuclear antigen of kaposi sarcoma-associated herpesvirus targets the retinoblastoma-E2F pathway and with the oncogene hras transforms primary rat cells. Cloutier N, Flamand L. Cyclin encoded by KS herpesvirus. Cancer Cell. Barton ES, et al. Herpesvirus latency confers symbiotic protection from bacterial infection. Chin YE, et al. Takaoka A, et al.

Interferon-inducible antiviral effectors. Senger K, et al. Gene repression by coactivator repulsion. Harada H, et al. Anti-oncogenic and oncogenic potentials of interferon regulatory factors-1 and Viral interferon regulatory factors. Interferon Cytokine Res. Viral ILinduced cell proliferation and immune evasion of interferon activity. Lee H, et al. Iwakiri D, Takada K. Bhattacharya S, et al. Lane DP. Hornung V, Latz E. Intracellular DNA recognition. Ranjan P, et al. Cytoplasmic nucleic acid sensors in antiviral immunity.

Trends Mol. DNA repair proteins affect the lifecycle of herpes simplex virus 1. Shin YC, et al. Wu ZH, Miyamoto S. Shuda M, et al. T antigen mutations are a human tumor-specific signature for Merkel cell polyomavirus. Seroepidemiology of human polyomaviruses. PLoS Pathog. Tolstov YL, et al. Human Merkel cell polyomavirus infection II.

MCV is a common human infection that can be detected by conformational capsid epitope immunoassays. Carter JJ, et al. Association of Merkel cell polyomavirus-specific antibodies with Merkel cell carcinoma. Pastrana DV, et al.

Quantitation of human seroresponsiveness to Merkel cell polyomavirus. Touze A, et al. Human Merkel cell polyomavirus infection I. MCV T antigen expression in Merkel cell carcinoma, lymphoid tissues and lymphoid tumors. Sastre-Garau X, et al. Merkel cell carcinoma of the skin: pathological and molecular evidence for a causative role of MCV in oncogenesis. Merkel cell polyomavirus and two previously unknown polyomaviruses are chronically shed from human skin.

Cell Host Microbe. Kwun HJ, et al. The minimum replication origin of merkel cell polyomavirus has a unique large T-antigen loading architecture and requires small T-antigen expression for optimal replication.

Allander T, et al. Identification of a third human polyomavirus. Gaynor AM, et al. Identification of a novel polyomavirus from patients with acute respiratory tract infections.

Case-control study of human papillomavirus and oropharyngeal cancer. Parkin DM, et al. Part I: cancer in Indigenous Africans-burden, distribution, and trends. The possible role of viruses in cancer. Opening remarks. Temin HM, Rubin H. Characteristics of an assay for Rous sarcoma virus and Rous sarcoma cells in tissue culture. Baltimore D. Temin HM, Mizutani S. Chang HW, et al. Transformation of chicken cells by the gene encoding the catalytic subunit of PI 3-kinase. Bishop JM. Nobel Lecture.

Retroviruses and oncogenes II. Weiss RA. The discovery of endogenous retroviruses. Ebbesen P. In: Viruses Associated with Human Cancer. Phillips LA, editor. Marcel Dekker; New York: Klein G. MIT Press; Characterization of a 54K dalton cellular SV40 tumor antigen present in SVtransformed cells and uninfected embryonal carcinoma cells.

T antigen is bound to a host protein in SVtransformed cells. Coevolution of endogenous betaretroviruses of sheep and their host. Life Sci. Contreras-Galindo R, et al. Human endogenous retrovirus K HML-2 elements in the plasma of people with lymphoma and breast cancer.

Urisman A, et al. Hohn O, et al. Lack of evidence for xenotropic murine leukemia virus-related virus XMRV in German prostate cancer patients. A cautionary tale of virus and disease. BMC Biol. Koch R. In: SourceBookofMedicalHistory. Clark DH, editor. Dover Publications, Inc; New York: Hill AB.

Environment and disease: association or causation? Herpes-type virus and chromosome marker in normal leukocytes after growth with irradiated Burkitt cells.

Ernberg I, Klein G. Arvin A, et al. Saemundsen AK, et al. Cancer Research Workforce. Partners in Cancer Research. What Are Cancer Research Studies. Research Studies. Get Involved. Cancer Biology Research. Cancer Genomics Research. Research on Causes of Cancer. Cancer Prevention Research. Cancer Treatment Research. Cancer Health Disparities. Childhood Cancers Research. Global Cancer Research. Cancer Research Infrastructure.

Clinical Trials. Frederick National Laboratory for Cancer Research. Bioinformatics, Big Data, and Cancer. Annual Report to the Nation. Research Advances by Cancer Type. Stories of Discovery. Milestones in Cancer Research and Discovery. Biomedical Citizen Science. Director's Message. Budget Proposal. Stories of Cancer Research. Driving Discovery. Highlighted Scientific Opportunities. Research Grants. Research Funding Opportunities.

Cancer Grand Challenges. Research Program Contacts. These can arise as a result of DNA damage or by the incorporation of non-complementary nucleotides during DNA synthetic processes.

Based upon the disparity between the infrequency of spontaneous mutations and the large numbers of mutations reported in human tumors, it has been postulated that cancers must exhibit a mutator phenotype, which would represent an early event in cancer progression. A mutator phenotype could be generated by mutations in genes that normally function to guarantee genetic stability.

These mutations presumably arise via DNA damage by environmental or endogenous agents, but it remains to be determined whether the acquisition of a mutator phenotype is a necessary event during tumor progression.

Abstract People are continuously exposed exogenously to varying amounts of chemicals that have been shown to have carcinogenic or mutagenic properties in experimental systems. Publication types Research Support, Non-U. Gov't Research Support, U. HHV-8 is transmitted through sex and appears to be spread other ways, such as through blood and saliva, as well. HHV-8 infection is life-long as with other herpes viruses , but it does not appear to cause disease in most healthy people.

Having a weakened immune system appears to be one such factor. In the US, almost all people who develop KS have other conditions that have weakened their immune system, such as HIV infection or immune suppression after an organ transplant. The number of people with KS has dropped in the US since peaking in the early s, most likely because of better treatment of HIV infection.

For more information on KS, see Kaposi Sarcoma. HHV-8 infection has also been linked to some rare blood cancers, such as primary effusion lymphoma. The virus has also been found in many people with multicentric Castleman disease , an overgrowth of lymph nodes that acts very much like and often develops into cancer of the lymph nodes lymphoma.

For more information, see Castleman Disease. Further study is needed to better understand the role of HHV-8 in these diseases. This cancer is found mostly in southern Japan, the Caribbean, central Africa, parts of South America, and in some immigrant groups in the southeastern United States.

HTLV-1 belongs to a class of viruses called retroviruses. Some of the new DNA genes can then become part of the chromosomes of the human cell infected by the virus. This can change how the cell grows and divides, which can sometimes lead to cancer.

This has greatly reduced the chance of infection through transfusion, and has also helped control the potential spread of HTLV-1 infection. MCV was discovered in in samples from a rare and aggressive type of skin cancer called Merkel cell carcinoma. Most people are infected with MCV at some point often in childhood , and it usually causes no symptoms. But in a few people with this infection, the virus can affect the DNA inside cells, which can lead to Merkel cell cancer.

Nearly all Merkel cell cancers are now thought to be linked to this infection. It is not yet clear how people become infected with this virus, but it has been found in a number of places in the body, including normal skin and saliva.

SV40 is a virus that usually infects monkeys. Some polio vaccines prepared between and were made from monkey cells and were later found to be contaminated with SV But the accuracy of these older studies has been questioned. Scientists have found that some lab animals, such as hamsters, developed mesotheliomas when they were intentionally infected with SV Researchers have also noticed that SV40 can make mouse cells grown in the lab become cancerous.