Background. Ionizing radiation is a lung carcinogen in a variety of settings, including after breast cancer radiation therapy. The authors explored whether cigarette smoking and breast cancer radiation therapy have a multiplicative effect on the risk of subsequent lung cancer. Methods. This case‐control study investigated women registered with primary breast cancer in the Connecticut Tumor Registry who developed a second malignancy between 1986 and 1989. Those diagnosed with a subsequent primary lung cancer were compared with those diagnosed with a subsequent nonsmoking, nonradiation‐related second malignancy, and age‐adjusted odds ratios were calculated with logistic regression. Results. No radiation effects were observed within 10 years of initial primary breast cancer. Among both smokers and nonsmokers diagnosed with second primary cancers more than 10 years after an initial primary breast cancer, radiation therapy was associated with a 3‐fold increased risk of lung cancer. A multiplicative effect was observed, with women exposed to both cigarette smoking and breast cancer radiation therapy having a relative risk of 32.7 (95% confidence interval [CI], 6.9–154). The radiation carcinogenic effect was observed only for the ipsilateral lung and not for the contralateral lung both in smokers and nonsmokers. Conclusions. Breast cancer radiation therapy, as delivered before 1980, increased the risk of lung cancer after ten years in nonsmokers, and a multiplicative effect was observed in smokers. For both smokers and non‐smokers, this effect was observed only for the ipsilateral lung and not the contralateral lung. Modern techniques, however, significantly decrease the radiation dose to the lungs, which may decrease the risk of lung cancer. Nonetheless, due to the available choices in early‐stage breast cancer treatment, current practices may need to be revised for young breast cancer patients who smoke. Cancer 1994: 73:1615–20.

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Adenomatous polyps (hereinafter referred to as adenomas) are known precursors of colorectal cancer. Cigarette smoking has been associated with adenomas but not with colorectal cancer, while alcohol and fat intake have been associated with both adenomas and cancer in some studies. Approximately 30 percent of patients with resected adenomas develop another adenoma within three years. This case-control study explores the association of cigarette smoking with adenoma recurrence. Between April 1986 and March 1988, we administered a questionnaire to colonoscoped patients aged 35 to 84 years in three New York City (NY, USA) practices. We compared 186 recurrent polyp cases (130 males, 56 females) and 330 controls (187 males, 143 females) who had a history of polypectomy but normal follow-up colonoscopy, by cigarette-smoking pack-years adjusted for possible confounders. Risk for a metachronous or recurrent adenoma was significantly greater in the highest quartile of smokers than in never-smokers among both men (odds ratio [OR] = 1.8, 95 percent confidence interval [CI] = 1.0-3.4) and women (OR = 3.6, CI = 1.7-7.6). Adjustment for time since smoking cessation reduced risk only slightly, as did adjustment for dietary fat intake, which itself remained significant. No association was found between alcohol intake and risk of recurrence. Cigarette smokers appear to have an elevated risk of adenoma recurrence that is not eliminated entirely by smoking cessation. Intervention trials that use adenoma recurrence as an endpoint should take smoking into account.

Oral cancer incidence is higher in individuals between the fifth and seventh decades of life, but some studies indicate a decreasing age trend. From the epidemiological point of view, alcohol consumption is associated with the emergence of oral cancer by interfering with mechanisms of DNA synthesis and repair. From a genetic standpoint, variant alleles in genes encoding the enzymes of alcohol (CYP2E1 and ADH) and acetaldehyde (ALDH2) metabolism may play an important role in the genesis of oral cancer. This study aimed to assess the relation of polymorphisms ADH1B (rs1229984 and rs2066702), ADH1C (rs698), ALDH2 (rs671) and CYP2E1 96bp insertion and the risk of squamous cell carcinoma of the mouth floor, as well as its clinicopathological and prognostic characteristics in relation to alcohol consumption. Our sample group was made of 301 patients, with 159 controls without a previous history of cancer and 142 patients with oral cancer. Genomic DNA was extracted from peripheral blood samples and genotypes were determined by PCR-RFLP. Our results suggest that the presence of ALDH2 Lys504 allele and 96bp insertion CYP2E1 were significantly associated with oral cancer risk. ADH1C gene Ile350 allele was associated with the presence of positive lymph nodes, and lymphatic invasion was related to the presence of polymorphic alleles ADH1B*1, ADH1C Ile350 and ALDH2 Lys504. In conclusion, these results reveal potential markers of oral cancer risk and behavior.