Interaction of HPV-18 and nitrosomethylurea in the induction of squamous cell carcinoma

Garrett, Lenora R.; Perez‐Reyes, Nuria; Smith, Patricia P.; McDougall, James K.

doi:10.1093/carcin/14.2.329

Cited by 51 publications

(30 citation statements)

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“…36,37 In addition, the combined action of HPV-18 and NMU in the induction of squamous cell carcinoma has been shown. 38 Our data on neoplastic transformation of HPV-18-immortalized HPE cells by exposure to NMU provides additional support for the theory that neoplastic conversion is a multistep process. This system may be useful in evaluating the carcinogenic potential of environmental chemicals for studying genes that are activated or suppressed in the multistep process leading to malignancy.…”

Section: In Vitro Human Cell Culture Models Js Rhimsupporting

confidence: 72%

In vitro human cell culture models for the study of prostate cancer

Rhim

2000

Prostate Cancer Prostatic Dis

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Prostate cancer is the most commonly diagnosed malignancy in the American men and the second leading cause of male cancer death in the United States. Despite its high incidence, the molecular and genetic events involved in prostate cancer progression remain poorly understood. A hurdle in understanding the molecular genetic changes in prostate cancer has been the dif®culty in establishing premalignant lesions and primary prostate tumors as in vitro cell cultures. Primary epithelial cells grow for a ®nite life span and then senesce. Immortalization is de®ned by continuous growth of otherwise senescing cells and is believed to represent an early stage in tumor progression. In order to examine these early stages, we and others have developed in vitro models of prostate epithelial cell immortalization. Because prostate cancer is a multistep, progressive disease with a typical onset later in life and with an unusually high number of latent cases that do not develop into clinically manifest cancer, the steps in the progression to malignancy are of particular interest. To understand the many factors that are suspected to contribute to the development of this malignancy, there is a need for an in vitro multistep human prostate epithelial (HPE) culture system. These models have been extremely important in identifying genetic and molecular changes involved in prostate cancer progression. Prostate Cancer and Prostatic Diseases (2000) 3, 229±235.

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Section: In Vitro Human Cell Culture Models Js Rhimsupporting

confidence: 72%

In vitro human cell culture models for the study of prostate cancer

Rhim

2000

Prostate Cancer Prostatic Dis

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“…Because it appears that it is most important if patients with cancer are current smokers at the time of diagnosis, current smoking likely has a promotional effect at late stages of disease progression. Garrett et al 26 found that HPV-18-immortalized human keratinocytes treated with a low dose of a compound similar to N-nitroso compounds found in tobacco and a single exposure to TPA, a tumor promoter, were converted to a malignant phenotype. It also has been shown that nicotine inhibits apoptosis, which may promote tumor growth.…”

Section: Discussionmentioning

confidence: 99%

Human papillomavirus, smoking, and sexual practices in the etiology of anal cancer

Daling

Madeleine

Johnson

et al. 2004

Cancer

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708

553

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BACKGROUNDThe incidence of anal cancer has increased among both men (160%) and women (78%) from 1973 to 2000 in the U.S. The authors conducted a population‐based case–control study of anal cancer to examine factors that may account for this increase.METHODSMen (n = 119 patients) and women (n = 187 patients) who were diagnosed with anal cancer between 1986 and 1998 in the Seattle area were ascertained through the local Surveillance, Epidemiology, and End Results registry. Control participants (n = 1700) were ascertained through random‐digit telephone dialing. Participants were interviewed in person and provided blood samples. Archival tumor tissue was tested for human papilloma virus (HPV) DNA, and serum samples were tested for HPV type 16 (HPV‐16).RESULTSOverall, 88% of tumors (all histologies) in the study were found to be positive for HPV. HPV‐16 was the most frequent HPV type detected (73% of all tumors), followed by HPV‐18 (6.9%), regardless of gender. However, 97.7% of tumors from men who were not exclusively heterosexual contained HPV DNA. The risk of anal cancer increased among men (odds ratio [OR], 5.3; 95% confidence interval [95% CI], 2.4–12.0) and women (OR, 11.0; 95% CI, 5.5–22.1) who had ≥ 15 sexual partners during their lifetime. Among men who were not exclusively heterosexual and women, receptive anal intercourse was related strongly to the risk of anal cancer (OR, 6.8 [95% CI, 1.4–33.8] and OR, 2.2 [95% CI, 1.4–3.3], respectively). Current smokers among men and women were at particularly high risk for anal cancer, independent of age and other risk factors (OR, 3.9 [95% CI, 1.9–8.0] and OR, 3.8 [95% CI, 2.4–6.2], respectively).CONCLUSIONSThe high proportion of tumors with detectable HPV suggests that infection with HPV is a necessary cause of anal cancer, similar to that of cervical cancer. Increases in the prevalence of exposures, such as cigarette smoking, anal intercourse, HPV infection, and the number of lifetime sexual partners, may account for the increasing incidence of anal cancer in men and women. Cancer 2004. © 2004 American Cancer Society.

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“…Epidemiological studies suggest that environmental and host-related cofactors act in conjunction with HPV to promote malignant progression of cervical lesions (7). It has been proposed that cigarette smoking among HPV-positive women is one of the cofactors which likely influences the risk for cervical cancer progression (15,21,27,38,41,50,52,54). Tobacco-specific polycyclic aromatic hydrocarbons such as benzo[a]pyrene (BaP) (31) and nitrosamines such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) (43), which are potent inducers of carcinogenesis (12,16,28), have been detected in the cervical mucus of women who smoke and exhibit cervical dysplasias (19,29,47).…”

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confidence: 99%

“…Quantitative levels of noncarcinogenic nicotine and its metabolite cotinine in cervical mucus were correlated with smoking intensity (29,47,48) and were shown to be concentrated more strongly in cervical mucus than in blood (17). Colocalization of HPV and cigarette smoke carcinogens in the cervix may present an opportunity for virus/ carcinogen interaction (15).…”

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confidence: 99%

The Cigarette Smoke Carcinogen Benzo[ a ]pyrene Enhances Human Papillomavirus Synthesis

Alam

Conway

Chen

et al. 2008

J Virol

103

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Epidemiological studies suggest that cigarette smoke carcinogens are cofactors which synergize with human papillomavirus (HPV) to increase the risk of cervical cancer progression. Benzo[a]pyrene (BaP), a major carcinogen in cigarette smoke, is detected in the cervical mucus and may interact with HPV. Exposure of cervical cells to high concentrations of BaP resulted in a 10-fold increase in HPV type 31 (HPV31) viral titers, whereas treatment with low concentrations of BaP resulted in an increased number of HPV genome copies but not an increase in virion morphogenesis. BaP exposure also increased HPV16 and HPV18 viral titers. Overall, BaP modulation of the HPV life cycle could potentially enhance viral persistence, host tissue carcinogenesis, and permissiveness for cancer progression.Worldwide, cervical cancer is the third most prevalent type of female cancer and ranks second as a cause of cancer-related deaths in women (49). Human papillomavirus (HPV) is causatively linked to over 90% of all cervical cancer cases examined (5,20,42,51,55). Most cases of HPV-induced dysplasia spontaneously regress over time (18), and only a small percentage of women infected with oncogenic "high-risk" HPV types, such as HPV type 16 (HPV16), HPV18, and HPV31, progress to high-grade squamous intraepithelial lesions and cervical cancer (4, 10). Epidemiological studies suggest that environmental and host-related cofactors act in conjunction with HPV to promote malignant progression of cervical lesions (7). It has been proposed that cigarette smoking among HPV-positive women is one of the cofactors which likely influences the risk for cervical cancer progression (15,21,27,38,41,50,52,54). Tobacco-specific polycyclic aromatic hydrocarbons such as benzo[a]pyrene (BaP) (31) and nitrosamines such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) (43), which are potent inducers of carcinogenesis (12,16,28), have been detected in the cervical mucus of women who smoke and exhibit cervical dysplasias (19,29,47). Quantitative levels of noncarcinogenic nicotine and its metabolite cotinine in cervical mucus were correlated with smoking intensity (29,47,48) and were shown to be concentrated more strongly in cervical mucus than in blood (17). Colocalization of HPV and cigarette smoke carcinogens in the cervix may present an opportunity for virus/ carcinogen interaction (15).Molecular mechanisms targeted by cigarette smoke carcinogens which potentially deregulate the HPV life cycle and which may promote cervical cancer progression have not been addressed. In this study, we demonstrate for the first time that BaP, a major carcinogenic constituent of cigarette smoke, stimulates high levels of virion synthesis in cell lines productively infected with HPV.We have previously demonstrated that the complete HPV life cycle is strictly dependent on host tissue differentiation (2,14,32,33,35,36,40). Utilizing the in vitro organotypic raft culture system and the CIN-612 9E cervical intraepithelial neoplasia type I biopsy-derived cell line, our laboratory ...

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Interaction of HPV-18 and nitrosomethylurea in the induction of squamous cell carcinoma

Cited by 51 publications

References 0 publications

In vitro human cell culture models for the study of prostate cancer

In vitro human cell culture models for the study of prostate cancer

Human papillomavirus, smoking, and sexual practices in the etiology of anal cancer

The Cigarette Smoke Carcinogen Benzo[ a ]pyrene Enhances Human Papillomavirus Synthesis

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