The health consequences of smoking: Cancer

Twenty cases of an unusual tumor of the lung are described. This tumor usually presents with multiple small, slowly growing pulmonary nodules. Many cases are detected incidentally. Eighty percent are women, and 50% are less than 40 years of age. Survival with tumor can be quite long. However, one half the patients have died, usually of progressive pulmonary insufficiency. This is a peculiar sclerosing tumor of endothelial cell origin.

Intravascular, bronchiolar, and alveolar tumor of the lung (IVBAT). An analysis of twenty cases of a peculiar sclerosing endothelial tumor.

The Epidemiology of Lung Cancer

Purpose People with HIV infection in the United States frequently smoke tobacco. We sought to characterize lung cancer incidence among HIV-infected individuals, examine whether cancer risk was related to HIV-induced immunosuppression, and assess whether the high prevalence of smoking explained elevated risk. Methods We conducted a retrospective cohort study at an HIV specialty clinic in Baltimore, MD (1989-2003). Incident lung cancers were identified using hospital records. We used negative binomial regression to compare incidence across subgroups defined by demographics, use of highly active antiretroviral therapy (HAART), and HIV markers. Standardized incidence ratios (SIRs) compared incidence with an urban reference population (Detroit, MI). We adjusted SIRs for the effect of smoking, using smoking prevalences estimated from part of the cohort and the general population. 95% CIs and P values were two sided. Results Thirty-three lung cancers were observed among 5,238 HIV-infected patients (incidence: 17...

Elevated Incidence of Lung Cancer Among HIV-Infected Individuals

Although only a subset of smokers develop lung cancer, we cannot determine which smokers are at highest risk for cancer development, nor do we know the signaling pathways altered early in the process of tumorigenesis in these individuals. On the basis of the concept that cigarette smoke creates a molecular field of injury throughout the respiratory tract, this study explores oncogenic pathway deregulation in cytologically normal proximal airway epithelial cells of smokers at risk for lung cancer. We observed a significant increase in a genomic signature of phosphatidylinositol 3-kinase (PI3K) pathway activation in the cytologically normal bronchial airway of smokers with lung cancer and smokers with dysplastic lesions, suggesting that PI3K is activated in the proximal airway before tumorigenesis. Further, PI3K activity is decreased in the airway of high-risk smokers who had significant regression of dysplasia after treatment with the chemopreventive agent myo-inositol, and myo-inositol inhibits the PI3K pathway in vitro. These results suggest that deregulation of the PI3K pathway in the bronchial airway epithelium of smokers is an early, measurable, and reversible event in the development of lung cancer and that genomic profiling of these relatively accessible airway cells may enable personalized approaches to chemoprevention and therapy. Our work further suggests that additional lung cancer chemoprevention trials either targeting the PI3K pathway or measuring airway PI3K activation as an intermediate endpoint are warranted.

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Airway PI3K Pathway Activation Is an Early and Reversible Event in Lung Cancer Development

In a review of 1,186 cases of lung cancer found amoung 7,629 autopsied cases over a 21 year period a total of 82 peripheral cancers related to scars were found, constituting 1% of the autopsied cases and 7% of the lung tumors. 15% of all lung tumors were peripheral (vs. bronchogenic) and the percentage rose from less than 7 in the time period of 1955 to 1960 to a little more than 23 in the 1970 to 1976 time period. 45% of all peripheral lung cancers originated in a scar. Less than 2% of all lung cancers were found associated with scars in the 1955 through 1959 time period. This increased to nearly 16% in the 1970 through 1975 time period. 72% of the scar cancers were adenocarcinomas and 18% were of squamous cell type. The rest were large cell undifferentiated carcinomas and none was oat cell or small cell type. Over three-quarters of these scar cancers were found in the upper lobes and more than half were related to infarcts. Less than a quarter were related to tuberculosis scars. No relationship was found between smoking habits and scar cancer.

Scar cancer of the lung: increase over a 21 year period.

Histologic changes in the larynx were microscopically studied in 942 men who died and came to autopsy at the Veterans Administration Hospital, East Orange, N. J., between 1964-1967. Atypical changes in cells in the epithelium of the larynx were most often observed in the true vocal cord and, to a lesser degree, in the false vocal cord and the area of the larynx above the vocal cord. The least changes were observed in the area below the vocal cord. The histologic changes (including cells with atypical nuclei, carcinoma in situ, and early invasive carcinoma) were highly related to smoking habits. They were much higher in cigarette smokers than in men who never smoked; they increased in proportion to the number of cigarettes smoked per day before death and were seen to a greater degree in cigarette smokers than in cigar and pipe smokers. Ex-cigarette smokers had fewer such changes than men who continued to smoke cigarettes up to the time of death. Cells with disintegrating nuclei were found mainly in ex-cigarette smokers.

https://acsjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/1097-0142%28197001%2925%3A1%3C92%3A%3AAID-CNCR2820250114%3E3.0.CO%3B2-E

Oscar Auerbach

Papers

Scar cancer of the lung: increase over a 21 year period.

Histologic changes in the larynx in relation to smoking habits.