The Genetics of Tobacco-Induced Malignancy

Davidson, Bruce J.; Hsu, Teng-Kuei; Schantz, Stimson P.

doi:10.1001/archotol.1993.01880230040007

Cited by 26 publications

(9 citation statements)

References 50 publications

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“…An excess of GSTµ(-) individuals among laryngeal cancer patients has previously been reported (Davidson et al 1993;Lafuente et al 1993) although those studies concerned heavy smokers and not alcoholics. As far as is known, no previous study has reported an excess frequency of GSTµ(-) individuals among oropharyngeal cancer patients, although such an excess has been reported for many other types of cancer (Di Ilio et al 1989;Howie et al 1989;Seidegard et al 1990;Shea et al 1990;Hayes PC et al 1991;Strange et al 1991;Zhong et al 1991;Bell et al 1992;Harada et al 1992;Hayachi et al 1992;Daly et al 1993;Davidson et al 1993;Hirvonen et al 1993;Kihara et al 1993;Nakachi et al 1993;Nazar-Stewart et al 1993;Anttila et al 1994;Heagerty et al 1994). …”

Section: Discussionmentioning

confidence: 96%

Laryngeal and oropharyngeal cancer, and alcohol dehydrogenase 3 and glutathione S-transferase M1 polymorphisms

et al. 1997

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In this study the GSTmu phenotype and ADH genotype at the ADH3 locus were investigated in a group of 39 alcoholic men with upper respiratory/digestive tract cancer: 21 with oropharyngeal cancer and 18 with laryngeal cancer. The results are compared with those of a control group of 37 alcoholic men without alcohol-related medical complications. Of the control subjects, 48% were found to be GSTmu deficient [GSTmu(-)] and 19% carried the ADH(3)1/ADH(3)1 genotype. In the laryngeal cancer patients, a significantly elevated frequency of both the GSTmu(-) (78%) and ADH(3)1/ADH(3)1 genotype (56%) was observed, relative to the control group. On the basis of this result, the risk of laryngeal cancer associated with the GSTmu(-) and ADH(3)1/ADH(3)1 genotypic combination within the population of alcoholics was estimated to be 12.9 with a 95% confidence interval of 1.8-92 (P < 0.01) relative to alcoholic individuals who have GSTmu [GSTmu(+)] and are not ADH(3)1/ADH(3)1. Thus, alcoholics who are GSTmu(-) and ADH(3)1/ADH(3)1 have at least an 80% greater risk of developing laryngeal cancer than alcoholics who are GSTmu(+) and who are not ADH(3)1/ADH(3)1. In addition, the oropharyngeal cancer patients had excess frequencies of both GSTmu(-) (62%) and ADH(3)1/ADH(3)1 (43%) relative to the control group, but these excess frequencies were not statistically significant. The GSTmu(-) and ADH(3)1/ADH(3)1 genotypic combination may be a constitutional risk factor for laryngeal cancer among alcoholics.

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Section: Discussionmentioning

confidence: 96%

Laryngeal and oropharyngeal cancer, and alcohol dehydrogenase 3 and glutathione S-transferase M1 polymorphisms

et al. 1997

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“…Tobacco use, like alcohol consumption, has a definite epidemiological association with the development of OSCC, suggesting an etiological role. Tobacco smoke contains toxic aldehydes, and the combined use of tobacco and alcohol has a synergistic effect on the risk of developing oral cancer (55). Homann et al (50) showed that tobacco smokers exposed to ethanol had a high concentration of salivary acetaldehyde.…”

Section: Attributes Of C Albicans That May Influence Oral Cancer Devmentioning

confidence: 99%

Revisiting the association between candidal infection and carcinoma, particularly oral squamous cell carcinoma

Bakri

Hussaini

Holmes

et al. 2010

Journal of Oral Microbiology

121

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BackgroundTobacco and alcohol are risk factors associated with cancer of the upper aerodigestive tract, but increasingly the role of infection and chronic inflammation is recognized as being significant in cancer development. Bacteria, particularly Helicobacter pylori, and viruses such as members of the human papilloma virus family and hepatitis B and C are strongly implicated as etiological factors in certain cancers. There is less evidence for an association between fungi and cancer, although it has been recognized for many years that white patches on the oral mucosa, which are infected with Candida, have a greater likelihood of undergoing malignant transformation than those that are not infected.ObjectiveThis article reviews the association between the development of oral squamous cell carcinoma in potentially malignant oral lesions with chronic candidal infection and describes mechanisms that may be involved in Candida-associated malignant transformation.

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“…These data support the contention that tumor progression depends not only on exposure to environmental carcinogens, particularly tobacco smoke, but also possibly on an inherited genetically defined sensitivity to mutagens. Hypersensitivity to bleomycin-induced mutagenesis may reflect an inherited defective DNA-repair capability in the host, with high susceptibility to the genotoxic effect of environmental carcinogens (such as tobacco and alcohol) (Hsu et al, 1989;Schantz et al, 1990;Parshad et al, 1993;Davidson et al, 1993). Thus, it is likely that subjects with increased susceptibility to carcinogens are at higher risk for malignant progression, particularly in the larynx, after exposure to tobacco and/or alcohol, capable of inducing genetic (Davidson et al, 1993) and morphological alterations of the exposed mucosae.…”

Section: Resultsmentioning

confidence: 99%

Increased mutagen-induced chromosome damage in patients with transformed laryngeal pre-cancerosis

et al. 1996

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Factors that contribute to malignant transformation of laryn-geal pre-neoplastic lesions remain largely unknown. Potential etiological factors may be related to a genetically controlled sensitivity to environmental carcinogens. In this study, we investigated bleomycin-induced chromosome damage in I5 patients who experienced a malignant transformation of pre-neoplastic laryngeal lesions during follow-up, as compared with chromosome fragility in 30 historical controls with no progression of keratoses during a 10-year follow-up, in a match-paired analysis. Chromosomal analysis demonstrated higher sensitivity to clastogens in patients with malignant progression of laryngeal pre-neoplastic lesions than that of control patients with no evolution of their original laryngeal keratoses (p = 0.003). Furthermore, among the study patients, chromosome sensitivity was most apparent in non-tobacco users with malignant transformation of laryngeal disease. Our data suggest that subjects with pre-neoplastic laryngeal lesion showing increased susceptibility to carcinogens could be at higher risk for development of laryngeal carcinoma. 8 1996 Wilq-Liss, Inc.

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The Genetics of Tobacco-Induced Malignancy

Cited by 26 publications

References 50 publications

Laryngeal and oropharyngeal cancer, and alcohol dehydrogenase 3 and glutathione S-transferase M1 polymorphisms

Laryngeal and oropharyngeal cancer, and alcohol dehydrogenase 3 and glutathione S-transferase M1 polymorphisms

Revisiting the association between candidal infection and carcinoma, particularly oral squamous cell carcinoma

Increased mutagen-induced chromosome damage in patients with transformed laryngeal pre-cancerosis

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