Oral cancer induced in hamsters with herpes simplex infection and simulated snuff dipping

Park, N.-H.; Sapp, J. Philip; Herbosa, Eugenio G.

doi:10.1016/0030-4220(86)90039-3

Cited by 52 publications

(14 citation statements)

References 20 publications

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“…However, continued intraoral placement of smokeless tobacco failed to evoke malignant conversion of oral mucosal cells of animals in vivo, indicating that tobacco use alone may not suffice development of oral cancer Park et al, 1986). Hence, other environmental factors including alcohol consumption, nutritional deficiencies, and DNA tumor viruses have also been implicated in oral carcinogenesis.…”

Section: Etiologic Factors Of Oral Cancermentioning

confidence: 99%

Genetic instability and oral cancer

Park¹,

Kang²

2000

Electron. J. Biotechnol.

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Development of oral cancer proceeds through discrete molecular genetic changes that are acquired from the loss of genomic integrity after continued exposure to environmental risk factors. Of particular importance in oral cancer development are tobacco-related chemical carcinogens and human papillomavirus (HPV) infection. To understand the mechanisms by which these risk factors contribute to tumorigenesis, we developed an in vitro model of sequential, multistep oral carcinogenesis model of normal human oral keratinocytes (NHOK) by immortalizing these cells with cloned "high risk" HPV genome. HPV viral genome alone failed to give rise to a tumorigenic cell population, which required further exposure to chemical carcinogens.HPV-immortalized cells exhibited impaired cell cycle control and DNA repair activity upon exposure to DNA damaging agents, and accumulated elevated frequency of spontaneous and mutagen-induced mutation. Furthermore, expression of E6 and E7 oncoproteins of "high risk" HPV were found to be sufficient for the enhanced mutation frequency in NHOK. These findings suggest that viral infection in combination with existing chemical carcinogens may be the paramount causative agents for the induction of genetic instability and development of oral cancer.

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Section: Etiologic Factors Of Oral Cancermentioning

confidence: 99%

Genetic instability and oral cancer

Park¹,

Kang²

2000

Electron. J. Biotechnol.

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“…Repeated intra-oral placement of smokeless tobacco (simulated snuff-dipping) has failed to produce malignant changes in the oral cavities of animals Park et al, 1986).…”

Section: (1) Tobacco-specific Chemical Carcinogensmentioning

confidence: 99%

“…Involvement of other contributing co-factors such as alcohol (Williams and Horm, 1977;Istvan and Matarazzo, 1984), nutritional deficiencies (Heimburger et al, 1988;Chen et al, 1989;Stich and Anders, 1989), and virus (Shillitoe et al, 1982;Park et al, 1985Park et al, , 1986Greer et al, 1990;Palefsky, 1991;Park, 1991) Percentages of cells (A, RKO; B, NHOK; C, SCC-9) at either GO/G1, S, or G2/M phases with or without 200 mM ethanol are shown. Ethanol treatment induced cell cycle arrest at G1 in all cells tested (Guo et al, 1997).…”

Section: (1) Tobacco-specific Chemical Carcinogensmentioning

confidence: 99%

Conversion of Normal To Malignant Phenotype: Telomere Shortening, Telomerase Activation, and Genomic Instability During Immortalization of Human Oral Keratinocytes

Kang

Park

2001

Critical Reviews in Oral Biology & Medicine

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shorten. In a few immortal clones surviving beyond the crisis, we found a marked elevation of telomerase activity and stabilization of telomere length. Furthermore, the E6 and E7 oncoproteins of "high risk" HPV disrupted the cell cycle control and DNA repair in immortalized HOK, and enhanced mutation frequency resulting from genomic instability. However, HPV infection alone failed to give rise to a tumorigenic cell population, which required further exposure to chemical carcinogens in addition to HPV infection. Analysis of the data presented suggests that oral carcinogenesis is a series of discrete genetic alterations that result from a continued genotoxic challenge by environmental risk factors. Our in vitro model may be useful for investigators with interest in furthering our understanding of oral carcinogenesis.

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“…This suggests a different course of an earlier herpetic infection in these patients with a prolonged exposure to early immediate HSVproteins which may be related to an increased risk of developing head and neck cancer. We propose that heavy smoking may contribute to this phenomenon.Numerous reports link herpes simplex virus (HSV) with cancer in humans (Shillitoe and Silverman, 1979;Rapp, 1980;Park et al, 1986;Aurelian et al, 1976;Maitland, 1988). Epidemiological studies have suggested a relationship, particularly between the presence of antibodies to HSV type 2 (HSV-2) and cancer of the uterine cervix (Nahmias and Norrild 1980;Rawls et al, 1969).…”

mentioning

confidence: 98%

“…Numerous reports link herpes simplex virus (HSV) with cancer in humans (Shillitoe and Silverman, 1979;Rapp, 1980;Park et al, 1986;Aurelian et al, 1976;Maitland, 1988). Epidemiological studies have suggested a relationship, particularly between the presence of antibodies to HSV type 2 (HSV-2) and cancer of the uterine cervix (Nahmias and Norrild 1980;Rawls et al, 1969).…”

mentioning

confidence: 99%

Reactivity against herpes simplex virus in patients with head and neck cancer

Pa¹,

Edström²,

Westin³

et al. 1991

Intl Journal of Cancer

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The relation between herpes simplex virus (HSV) and head and neck cancer was examined. A total of ninety patients were analyzed for IgG antibodies against HSV. Antibody titers were established with an enzyme-linked immunosorbent assay and antibodies against specific HSV-antigens were analyzed by Western blot. These patients' seroreactivity was compared to that of an age-matched control group of patients with arteriosclerotic disease in their lower limbs, a disease also closely related to heavy tobacco consumption. Prevalence of antibodies against HSV was around 90% and did not differ significantly between cancer patients and controls, but antibody titers against HSV were significantly higher in the cancer patients. The cancer patients also reacted more constantly (80%) in Western blot analysis against the early immediate protein, ICP-4, than controls (50%). This suggests a different course of an earlier herpetic infection in these patients with a prolonged exposure to early immediate HSV-proteins which may be related to an increased risk of developing head and neck cancer. We propose that heavy smoking may contribute to this phenomenon.

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Oral cancer induced in hamsters with herpes simplex infection and simulated snuff dipping

Cited by 52 publications

References 20 publications

Genetic instability and oral cancer

Genetic instability and oral cancer

Conversion of Normal To Malignant Phenotype: Telomere Shortening, Telomerase Activation, and Genomic Instability During Immortalization of Human Oral Keratinocytes

Reactivity against herpes simplex virus in patients with head and neck cancer

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