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All incident cases of microscopically confirmed lung cancer diagnosed between 1974 and 1981 in western Washington State were ~dentified through the sur~eillance, Epide- miology, ~ and End Results Program of the Na- tional Cancer Institute, Bethesda, MD. The incidence of lung cancer by histologic type was studied in relation to time, with age, sex, and stage of disease at diagnosis be- ing taken into account. Overall and within each sex, the incidence of adenocarcinoma has increased significantly since 1974. The rate of increase has been higher among fema- les (86% increase) than among males (54% increase), with most of the increase in both sexes being among those over age 65 years with distant or unstaged disease at diagno- sis. Similar patterns were not observed for squamous cell carcinoma. The potential ef- fects of changes in diagnostic and patholo- gy practice during the study period in pro- ducing these results were explored, and eti- ologic implications of the observed increase in adenocarcinoma were discussed.

Increased Familial Risk for Lung Cancer. ooi, W.L., Elston, R.C., Chen, V.W. et al. Department of Medicine, Louisiana State Uni- versity Medical Center, New Orleans, LA 70112, U.S.A.J. Natl. Cancer Inst. 76: 217- 222, 1986.

For the determination of whether lung cancer clusters in families, an analysis was conducted on demographic and morbidity- mortality data, occupational and industrial experiences, and tobacco use practices for family members of 336 deceased lung cancer probands and 307 controls (probands' spou- ses). First-degree relatives of probands, compared with first-degree relatives of con- trols, showed a strong excess risk for lung cancer. Overall, male relatives of probands had a greater risk for lung cancer than did their female counterparts, and the risk was fourfold for parents of probands as compa- red with parents of spouses. Female rela- tives of probands over 40 years old were at nine times higher risk than similarly aged female controls, even among those who were nonsmokers and who had not reported excessive exposure to hazardous occupations; the risk was fourfold to sixfold for heavy smokers. After control for the confounding effects of age, sex, cigarette smoking, and occupational and industrial exposures, re- lationship to proband remained a significant determinant of lung cancer, with a 2.4-fold greater risk among relatives of probands.

Genetics and Smoking-Associated Cancer: A Study of 485 Families. Lynch, H.T., Kimberling, W.J., Markvicka, S. E. et al. Department of Preventive Medicine, Creighton University School of Medicine,

Omaha, NE 68178, U.S.A. Cancer 57: 1640-1646, 1986.

Cancer risk was evaluated in relatives of 254 consecutively ascentained probands with histologically verified lung cancer, and 231 probands with other smoking-related can- cers. Findings disclosed a lack of any strong evidence for increased risk in lung cancer per se when only lung cancer in relatives was considered. Confounding factors, most prominent of which was the effect of ciga- rette smoking, variation of secular trends, and the heritability of the smoking pheno- type itself, tended to obfuscate identifica- tion of an inherited effect presenting itself exclusively as lung cancer liability. On the other hand, a significant increase was ob- served in cancers of all anatomic sites among the relatives of lung cancer probands (P<0.001). Most of these neoplastic lesions were not associated with smoking and were not greatly influenced by secular trends. Further- more, no significant excesses of cancer at all anatomic sites in relatives of probands with other smoking-associated carcinomas we- re observed. Thus, it may be concluded that the observation of increased risk for cancer at all anatomic sites in relatives of lung cancer probands may be a reflection of an underlying susceptibility to malignancy in these families.

Mechanism of B enzoCa)Pyrene Induction of Alpha-H~nan Chorionic Gonadotropin Gene Ex- pression in H~nan Lung Tumor Cells. wong, D.T.W., Biswas, D.K. Laboratory of Pharmacology, Harvard School of Dental Me- dicine, Boston, MA 02115, U.S.A.J. Cell. Biol. i01: 2245-2252, 1985.

Human lung cells (ChaGo) derived from a bronchogenic carcinoma synthesize and secre- te in the culture medium the alpha subunit of the glycoprotein hormone, human chorionic gonadotropin (alpha-hCG). The synthesis of alpha-hCG by ChaGo cells could be further stimulated by treatment with sublethal con- centrations of the polycyclic aromatic hy- drocarbons (PAHs), benzo(a)pyrene (BaP), or dimethylbenzanthracene. The production of alpha-hCG could be correlated to the levels of alpha-hCG-specificmRNA sequences in con- trol and PAH-treated cells. Further analysis of the RNA species (Northern blot) revealed that the level of the mature (approx. 1.0 kb) and the high molecular weight alpha-hCG spe- cific nuclear TNA sequences (approx. 2.2 and 5 kb) were al~_qreater in PAH-treated cells. Addition of (-B)BaP (0.25 mug/ml) in the cul- ture medium of ChaGo cells led to immediate uptake of the radioactive compound apparent- ly by simple diffusion. SDS PAGE and subse- quent fluorography revealed that the radio- active compound interacted and formed cova- lent complexes with cytoplasmic and nuclear p~teins. This covalent interaction of the (--)BaP molecule with cellular proteins could

be significantly inhibited by either inhibi-