Cigarette Smoking and Dysplasia and Carcinoma In Situ of the Uterine Cervix

Trevathan, Edwin; Layde, Peter M.; Webster, Linda A.; Adams, M. Jacob; Benigno, Benedict B.; Ory, Howard W.

doi:10.1001/jama.1983.03340040039028

Cited by 101 publications

(19 citation statements)

References 11 publications

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“…Surprisingly, in view of the current viral and mutational theories, smoking was already known in the 1970s to induce cervical carcinomas [27,80-83]. In 1983 a study of the Centers for Disease Control even proved that “12 or more pack-years smoked” increase cervical carcinoma rates 12.4-fold compared to non-smokers [79]. The steady decline of cervical cancer in parallel with declining smoking rates in the US supports this theory [38].…”

Section: Discussionmentioning

confidence: 99%

“…The relevance of this theory to cervical carcinomas is supported by: (1) A plethora of classic evidence for abnormal DNA contents or aneuploidies in cervical carcinomas [1-21,64-67], (2) Recent evidence that the copy numbers of the mRNAs of individual carcinomas [33,45,68-72], like those of other cancers [73-78], are proportional to the copy numbers of the corresponding carcinoma-specific chromosomes (See Results regarding transcriptomes of cervical carcinomas), and (3) Induction of cervical carcinomas by aneuploidogenic cigarette smoke-carcinogens as predicted by the speciation theory [27,79-83]. …”

Section: Introductionmentioning

confidence: 99%

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Individual karyotypes at the origins of cervical carcinomas

et al. 2013

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BackgroundIn 1952 Papanicolaou et al. first diagnosed and graded cervical carcinomas based on individual “abnormal DNA contents” and cellular phenotypes. Surprisingly current papilloma virus and mutation theories of carcinomas do not mention these individualities. The viral theory holds that randomly integrated, defective genomes of papilloma viruses, which are often untranscribed, cause cervical carcinomas with unknown cofactors 20–50 years after infection. Virus-free carcinomas are attributed to mutations of a few tumor-suppressor genes, especially the p53 gene. But the paradox of how a few mutations or latent defective viral DNAs would generate carcinomas with endless individual DNA contents, degrees of malignancies and cellular phenotypes is unsolved. Since speciation predicts individuality, we test here the theory that cancers are autonomous species with individual clonal karyotypes and phenotypes. This theory postulates that carcinogens induce aneuploidy. By unbalancing mitosis genes aneuploidy catalyzes chain reactions of karyotypic evolutions. Most such evolutions end with non-viable karyotypes but a few become new cancer karyotypes. Despite congenitally unbalanced mitosis genes cancer karyotypes are stabilized by clonal selections for cancer-specific autonomy.ResultsTo test the prediction of the speciation theory that individual carcinomas have individual clonal karyotypes and phenotypes, we have analyzed here the phenotypes and karyotypes of nine cervical carcinomas. Seven of these contained papilloma virus sequences and two did not. We determined phenotypic individuality and clonality based on the morphology and sociology of carcinoma cells in vitro. Karyotypic individuality and clonality were determined by comparing all chromosomes of 20 karyotypes of carcinomas in three-dimensional arrays. Such arrays list chromosome numbers on the x-axis, chromosome copy numbers on the y-axis and the number of karyotypes arrayed on the z-axis. We found (1) individual clonal karyotypes and phenotypes in all nine carcinomas, but no virus-specific markers, (2) 1-to-1 variations between carcinoma-specific karyotypes and phenotypes, e.g. drug-resistance and cell morphology, (3) proportionality between the copy numbers of chromosomes and the copy numbers of hundreds of over- and under-expressed mRNAs, (4) evidence that tobacco-carcinogens induce cervical carcinomas via aneuploidy, consistent with the speciation theory.ConclusionsSince the individual clonal karyotypes of nine carcinomas correlated and co-varied 1-to-1 with complex individual transcriptomes and phenotypes, we have classical genetic and functional transcriptomic evidence to conclude that these karyotypes encode carcinomas - much like the clonal karyotypes that encode conventional species. These individual karyotypes explain the individual “DNA contents”, the endless grades of malignancies and the complex individual transcriptomes and phenotypes of carcinomas.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Individual karyotypes at the origins of cervical carcinomas

et al. 2013

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“…The final histological diagnoses were no neoplasia (15 patients), cervical intraepithelial neoplasia grade I (19), cervical intraepithelial neoplasia grade II (28), cervical intraepithelial neoplasia grade III (108), and microinvasive carcinoma (11). The patients were aged 20-67 with a mean age of 34-4 (SD 7 9) years.…”

Section: Diagnosesmentioning

confidence: 99%

Cigarette smoking and human papillomavirus in patients with reported cervical cytological abnormality.

Burger¹,

Hollema²,

Gouw³

et al. 1993

BMJ

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“…Most studies show that there is a strong correlation between women with cervical neoplasia and those who currently smoke 28,29. Current smoking (even passive smoking) has been linked to a 2-fold increase in the risk of developing cervical cancer 30,31.…”

Section: Discussionmentioning

confidence: 99%

Associations between Smoking, Screening, and Death Caused by Cervical Cancer in Korean Women

et al. 2007

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PurposeCervical cancer is a major women's health problem in the world today. The purpose of this study was to estimate the incidence and mortality rates and to investigate risk factors for cervical cancer in Korean women.Materials and MethodsReproductive factors, cigarette smoking, as well as the risk of incidence and death from cervical cancer were examined in a 12-year prospective cohort study of 475,398 Korean women aged 30 to 95 years who received health insurance from the National Health Insurance Corporation and who had a medical evaluation in 1992. Relative risks (RR) and 95% confidence intervals (CI) were calculated using the Cox proportional hazards model after adjusting for age, body mass index, cigarette smoking, alcohol use, menarche, parity, and Papanicolaou test status.ResultsThis study showed that the RR of death due to cervical cancer among current smokers was two times higher compared with non-smokers (RR = 2.00; 95% CI, 1.23-2.91). In addition, the RR of death due to cervical cancer among all women who smoked ≥ 10 cigarettes/day was 2.4 times higher than the RR among women that had never smoked. More interestingly, those who had never been screened by Papanicolaou smears had twice the risk of death due to cervical cancer (RR = 2.00; 95% CI, 1.37-1.81).ConclusionOur prospective study concluded that current smokers had an increased risk of death due to cervical cancer. We suggest that the target age group for cervical cancer screening tests be reconsidered and should begin as early as possible.

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Cigarette Smoking and Dysplasia and Carcinoma In Situ of the Uterine Cervix

Cited by 101 publications

References 11 publications

Individual karyotypes at the origins of cervical carcinomas

Individual karyotypes at the origins of cervical carcinomas

Cigarette smoking and human papillomavirus in patients with reported cervical cytological abnormality.

Associations between Smoking, Screening, and Death Caused by Cervical Cancer in Korean Women

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