ELSEVIER Lung Cancer 11 (1994) 123-150

Abstracts

Prevention

Cigarette smoking is a determinant of DT-diaphorase gene expression in human non-small cell lung carcinoma Gasdaska PY, Powis G, Hyman P, Fisher H. Arizona Cancer Center, 1515N. CampbellAwt,ue. Tucson,AiX5724. CancerRes 1993;53:5458- 61.

The levels of NAD(P)H:(quinone-acceptor) oxidoreductase (EC, I .6.99.2) (DT- diaphorase) mRNA and enzymeactivity havebeen studied in paired human normal lung and non-small cell lung tumor samples from patients with a history of cigarette smoking. There were significantly higher levels of DT-diaphorase mRNA (1.2 kilobases) in lung tumor compared to normal lung tissue of patients who had stopped smoking more than 6 months before surgery, with relative values (normalized to D-actin mRNA) of 29.6 f 7.8 (SE) in the lung tumor compared to 11.7 f 2.2 in normal lung tissue (P < 0.05). There was no significant difference in DT-diaphorase mRNA between lung tumor and normal lung tissue of subjects who were smokers at the time of surgery, with values of 16.5 f 2.1 and 15.3 f 2.5 (P > 0.05). respectively. DT-diaphorase enzyme activity in normal and tumor lung tissuewaspositively correlated with DT-diaphorasemRNA (r = 0.908, P < 0.01). The results of the study suggest that DT-diaphorase does not function as an inducible protectant enzyme in human lung against oxidant species and carcinogens present in cigarette smoke. Metabolism of some anticancer drugs by DTdiaphorase can alter their activity. Differences in DTdiaphorase between lung tumors of smokers and past smokers might alter the response to these drugs.

Risk factors of lung cancer by histological category in Taiwan Ger L-P, Hsu W-L, Chen K-T, Chen C-J. Department of Medical Research. T&Service General Hospital. Taipei. Anticancer Res 1993; 13:1491-1500.

The relationship between various risk factors and lung cancer by different histological typeswasevaluatedinacase~ntrolstudy. Atotal of 72 adenocarcinoma patients and 59 squamous/small cdl lung cancer patients, 262 hospital controls and 262 neighborhood controls were interviewed. Multiple conditional logistic regression analysis revealed that occupational exposures to asbestos and working as a cook were sis@kant risk factors associated with adenocarcinoma of the hmg. An inverse association between incense burning and the ad~~mo~ was noted. The squamous and small cell carcinomas of the lung were significantlyassociPtedwithcigarettes~g,psssivesmoLingexposure from friends at entertainment activities, the use of coal as cooking fuel, history of prior tuberculosis and chronic bronchitis, and occupational exposures to asbestos.

Rising lung cancer mortality in the United States, 19684988: The manifestation of altered disease competition Riggs JE. Department of Neurology, West Virginia University, School of Medicine, Morgantown, WV 265&I Regul Toxicol Pharmacol 1993;18:261-74.

Lung cancer mortality is increasing. The strong association between cigarette smoking and lung cancer is universally acknowledged. Consequently, rising lung cancer mortality is commonly attributed to cigarette smoking. This chain of logic has resulted in a remarkable evolution of public attitudes toward cigarette smoking and in increased regulationofsmdringatworkandinpublicplaces. However, longitudii Gompertxian analysis indicates that the major force increasing lung cancer mortality in the United States is the declining competitiveness of other causes of death, particularly ischemic heart disease and stroke. Indeed, this analysis demonstrates that the ‘environmental’ influence upon lung cancer mortality began to decline in the United States in the mid-197Os, supportingtheeffectiveneasofprogramsaimedatdecreasing tobacco use.

Are female smokers at higher risk for lung cancer than male smokers? A case-control analysis by histologic type Risch HA, Howe GR, Jain M, Burch JD, Holowaty EJ, Miller AB. Dept, ofEpiakmiology/PublicHedth, Yale VniversitySchoolofMedicine, 6OCoUegeStrtw, NewHawn, CT@BlO. AmJEpidemiol1993;138:281- 93.

A case-control study of male-female differences in cigarette smoking and lung cancer was conducted during 1981-1985 in Toronto, St. Catharine’s, and Niagara Falls, Gntario, Canada. In total, 442 female and 403 male histologically verified cancer cases were individually matched byageandareaofreaidenctoeachotherandto410 femaleand 362 male randomly selected population controls. Subjects were inter- viewed concerning their exposures to various life-style factors, and in particular, they received detailed questioning regarding their lifelong histories of usage of tobacco products. It was found that, for both sexes, a greatly elevated risk of developing lung cancer was associated with cigarette consumption, increasing with pack-years of cigarettes smoked anddeclining withdurationoftimesicequitting smoking. Furthermore, the association was significantly @ = 0.010) and appreciably stronger for females than for males. At a history of 40 pack-years relative to lifelong nonsmoking, the odds ratio for women was 27.9 (95% confidence interval (CI) 14.9-52.0) and that for men was 9.60 (95% CI 5.64-16.3). Higher odds ratios for females were also seen within each of the major histologic groupings. Thus, the higher elevated risk of lung