Viruses, chemicals and co-carcinogenesis

Haverkos, Harry W.

doi:10.1038/sj.onc.1207822

Cited by 42 publications

(23 citation statements)

References 83 publications

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“…28 years, which suggests in most cases a long precancerous state that allows the accumulation of secondary genetic changes. Although secondary genetic changes may occur randomly, the presence of tobacco metabolites in cervical secretions is considered a risk factor in the development of cervical cancer [158], with certain smoking carcinogens being found at significantly higher levels in the cervical secretions of cigarette-smoking women [159]. Multiparity and the long-term use of oral contraceptives are also associated with increased risk [160,161].…”

Section: Molecular Events During Cancer Progressionmentioning

confidence: 99%

Molecular biology of human papillomavirus infection and cervical cancer

Doorbar¹

2006

Clinical Science

872

701

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HPVs (human papillomaviruses) infect epithelial cells and cause a variety of lesions ranging from common warts/verrucas to cervical neoplasia and cancer. Over 100 different HPV types have been identified so far, with a subset of these being classified as high risk. High-risk HPV DNA is found in almost all cervical cancers (>99.7%), with HPV16 being the most prevalent type in both low-grade disease and cervical neoplasia. Productive infection by high-risk HPV types is manifest as cervical flat warts or condyloma that shed infectious virions from their surface. Viral genomes are maintained as episomes in the basal layer, with viral gene expression being tightly controlled as the infected cells move towards the epithelial surface. The pattern of viral gene expression in low-grade cervical lesions resembles that seen in productive warts caused by other HPV types. High-grade neoplasia represents an abortive infection in which viral gene expression becomes deregulated, and the normal life cycle of the virus cannot be completed. Most cervical cancers arise within the cervical transformation zone at the squamous/columnar junction, and it has been suggested that this is a site where productive infection may be inefficiently supported. The high-risk E6 and E7 proteins drive cell proliferation through their association with PDZ domain proteins and Rb (retinoblastoma), and contribute to neoplastic progression, whereas E6-mediated p53 degradation prevents the normal repair of chance mutations in the cellular genome. Cancers usually arise in individuals who fail to resolve their infection and who retain oncogene expression for years or decades. In most individuals, immune regression eventually leads to clearance of the virus, or to its maintenance in a latent or asymptomatic state in the basal cells.

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Section: Molecular Events During Cancer Progressionmentioning

confidence: 99%

Molecular biology of human papillomavirus infection and cervical cancer

Doorbar¹

2006

Clinical Science

872

701

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“…Co-carcinogens are chemical substances that cannot induce cancer when they are administered alone, but can enhance the carcinogenic effect of other substances. In general, co-carcinogens act as promoters in tissues in which the initiation stage has appeared (Haverkos, 2004). As can be seen from Table 2 the carcinogens are mainly related to lung cancer.…”

Section: Risk Assessmentmentioning

confidence: 89%

Risk of Air Pollution in Relation to Cancer in the Nordic Countries

Fauser¹,

Ketzel²,

Becker³

et al. 2016

TemaNord

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“…by enhancing the cellular proliferation or disturbing the immune system. 14–16 To aid in the risk assessment of ENM carcinogenicity, we provide an overview of the current carcinogenesis paradigm in vivo and in vitro (Figure 1). …”

Section: Overview Of Carcinogenesismentioning

confidence: 99%

Carcinogenic potential of high aspect ratio carbon nanomaterials

Luanpitpong

Wang

Davidson

et al. 2016

Environ. Sci.: Nano

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Engineered nanomaterials, including high aspect ratio carbon nanomaterials, are often commercialized without a complete human risk assessment and safety evaluation. A health concern has been raised that high aspect ratio nanomaterials such as carbon nanotubes may cause unintended health consequences, such as asbestos-like lung cancer and mesothelioma, when chronically inhaled. Considering the widespread industrial and clinical applications and the increasing incidence of human exposure to nanomaterials, it is important to address the issue of nanomaterial carcinogenicity in a timely manner. This review summarizes recent advances in nanomaterial genotoxicity and carcinogenicity with a focus on high aspect ratio carbon nanotubes, and discusses current knowledge gaps and future research directions.

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Viruses, chemicals and co-carcinogenesis

Cited by 42 publications

References 83 publications

Molecular biology of human papillomavirus infection and cervical cancer

Molecular biology of human papillomavirus infection and cervical cancer

Risk of Air Pollution in Relation to Cancer in the Nordic Countries

Carcinogenic potential of high aspect ratio carbon nanomaterials

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