The anatomical approach to the study of smoking and bronchogenic carcinoma.a preliminary report of forty-one cases

Auerbach, Oscar; Petrick, Thomas G.; Stout, Arthur Purdy; Statsinger, Arnold L.; Muehsam, Gerald E.; Forman, Jerome B.; Gere, J. Brewster

doi:10.1002/1097-0142(195601/02)9:1<76::aid-cncr2820090106>3.0.co;2-d

Cited by 71 publications

(16 citation statements)

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“…As squamous metaplasia occurred in the first week in guinea-pigs and in the second week in rats after the intra-pulmonary inoculation of cigarette condensate, it can be deduced that cigarette condensate has a very rapid and deleterious effect on the bronchial mucous membrane, destroying the ciliated epithelium and thus favouring the retention, in the bronchial mucosa, of any carcinogenic substance whether that be derived from cigarette smoke or from other sources such as atmospheric pollution. Similar changes have been reported in human lungs by Auerbach et al (1956Auerbach et al ( , 1957 and by Hamilton et al (1957) who have reported that metaplasia and other retrogressive epithelial changes in the bronchial epithelium were commoner in the lungs of smokers as compared with non-smokers. Chang (1957) also noted that basal cell multiplication was more marked, the average thickness of the bronchial mIucous membrane was greater and metaplasia more frequent in smokers than in non-smokers and that the average age of maximum frequency of these changes was from 50 to 69 years of age.…”

Section: Discussionsupporting

confidence: 86%

An Experimental Study of the Pathological Effects of Cigarette Condensate in the Lungs with Special Reference to Carcinogenesis

Blacklock

Cancer

1962

Journal of Occupational and Environmental Medicine

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Section: Discussionsupporting

confidence: 86%

An Experimental Study of the Pathological Effects of Cigarette Condensate in the Lungs with Special Reference to Carcinogenesis

Blacklock

Cancer

1962

Journal of Occupational and Environmental Medicine

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“…In 1956, Oscar Auerbach and colleagues published the first of a series of careful histologic investigations of the effects of tobacco smoke exposure on airway epithelium (116). The histologic grading system used was somewhat different than the current WHO/ IASLC grading system, but many of these findings from rapidly processed autopsies are still highly relevant (21).…”

Section: Bronchial Epithelial Damage In Smokersmentioning

confidence: 99%

Pathogenesis of Lung Cancer

Miller

2005

Am J Respir Cell Mol Biol

129

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Over the past 100 years, our understanding of the pathogenesis of lung cancer has advanced impressively. Environmental carcinogens and a gene locus determining susceptibility have been identified. The pathology of lung cancer has been classified into categories with major clinical implications. The cellular and molecular genetic changes underlying lung cancer have become better understood over the past 25 years, but the stepwise progression of respiratory epithelium from normal to neoplastic is not yet well demarcated, limiting abilities to advance early detection and chemoprevention. The translation of improved understanding of dominant signal transduction pathways in lung cancer to rationally designed therapeutic strategies has had recent successes, demonstrating a proof of principle for targeted therapy in lung cancer. Improvement in overall patient outcomes has been stubbornly slow and will require concerted efforts.

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“…A series of studies were done comparing the extent of hyperplasia and other bronchial lesions upon autopsy of men with varying histories of smoking who had died of causes other than lung cancer, as well as some biopsies and autopsies from smokers who had lung cancer (Auerbach et al, 1956(Auerbach et al, , 1961(Auerbach et al, , 1962. Data from the last of these studies is abstracted in Table 6.…”

Section: Precancerous Pulmonary Lesions Among Smokersmentioning

confidence: 99%

Selective clonal expansion and microenvironmental permissiveness in tobacco carcinogenesis

Rubin

2002

Oncogene

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Historically our knowledge about the direct carcinogenic activity of cigarette smoke and its constituents grew from painting experiments on the skin of mice to produce papillomas and carcinomas. The neutral fraction of cigarette smoke condensate had most of the carcinogenic activity in this test and was rich in carcinogenic polycyclic aromatic hydrocarbons (PAHs), the most abundant by far being BP. However, the concentration of BP in the condensate was only about 2% the amount of pure BP required to cause skin tumors. In other fractions there were non-carcinogenic constituents that promoted tumor formation when applied repeatedly to mouse skin that had been initiated by a single subcarcinogenic application of BP. There were also constituents of cigarette smoke that acted as cocarcinogens when applied simultaneously with repeated applications of BP. BP was effective as an initiator at lower concentrations than as a complete carcinogen, and some non-carcinogenic PAHs in the condensate were also active initiators. It was concluded from these studies that cigarette smoke condensate is primarily a tumorpromoting and co-carcinogenic agent with weak activity as a complete carcinogen. A major effect of promoters, and possibly of co-carcinogens, is a diffuse hyperplasia which includes selective expansion of clones carrying endogenous mutations and/or mutations induced by PAHs and other carcinogens such as NNK. The induced mutations as well as damaged cells would occur throughout the exposed region and, along with the hyperplasia, increase the permissiveness of the cellular microenvironment for neoplastic expression of any potential tumor cell in its midst. Since neither the promoters nor co-carcinogens in tobacco smoke are known to interact directly with DNA, their effects can be considered epigenetic processes that act upon genetically altered cells. Examples are cited from studies of experimental skin carcinogenesis, smoking-induced histopathological changes in human lung and spontaneous transformation in cell culture to illustrate the genetic and epigenetic interactions of neoplastic development in general and their significance for smoking-induced lung cancer in particular. Certain dietary modifications that appear to be effective in moderating the promotional phase of animal and human carcinogenesis are suggested for trial in managing lung cancer.

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The anatomical approach to the study of smoking and bronchogenic carcinoma.a preliminary report of forty-one cases

Cited by 71 publications

References 0 publications

An Experimental Study of the Pathological Effects of Cigarette Condensate in the Lungs with Special Reference to Carcinogenesis

An Experimental Study of the Pathological Effects of Cigarette Condensate in the Lungs with Special Reference to Carcinogenesis

Pathogenesis of Lung Cancer

Selective clonal expansion and microenvironmental permissiveness in tobacco carcinogenesis

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