Although exposure to estrogen may directly influence or modify the association between cigarette smoking and lung cancer risk, results from epidemiologic studies examining the association between reproductive and hormonal factors and risk of lung cancer among women have been inconsistent. Between 1998 and 2008, 430 women diagnosed with nonsmall cell lung cancer, 316 hospital controls and 295 population controls were recruited into the multi-center Maryland Lung Cancer Study. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) according to reproductive and hormonal exposures adjusting for age, smoking, passive smoking, education and household income. Results were similar for hospital and population based controls, so the control groups were combined. Reduced risks of lung cancer were observed among women with greater parity ( 5 vs. 1-2 births: OR 5 0.50, 95% CI 5 0.32, 0.78, p-trend 5 0.002) and later ages at last birth ( 30 vs. <25 years old: OR 5 0.68, 95% CI 5 0.48, 0.98, p-trend 5 0.04). After mutual adjustment parity, but not age at last birth, remained significantly inversely associated with risk (p-trend 5 0.01). No associations were found for nonsmall cell lung cancer risk with age at menarche, age at first birth, menopausal status, oral contraceptive use or menopausal hormone use, including use of oral estrogens. Compatible with findings from recent epidemiologic studies, we observed a reduction in the risk of nonsmall cell lung cancer with increasing number of births. Other reproductive and hormonal exposures, including menopausal hormone therapy use, were not associated with risk.

Cell cycle checkpoints play critical roles in the maintenance of genomic integrity. The inactivation of checkpoint genes by genetic and epigenetic mechanisms is frequent in all cancer types, as a less-efficient cell cycle control can lead to genetic instability and tumorigenesis. In an on-going case-control study consisting of 216 patients with non-small cell lung cancer, 226 population-based controls, and 114 hospital-based controls, we investigated the relationship of ;-radiationinduced G 2 -M arrest and lung cancer risk. Peripheral blood lymphocytes were cultured for 90 hours, exposed to 1.0 Gy ;-radiation, and harvested at 3 hours after ;-radiation treatment. ;-Radiation-induced G 2 -M arrest was measured as the percentage of mitotic cells in untreated cultures minus the percentage of mitotic cells in ;-radiation-treated cultures from the same subject. The mean percentage of ;-radiation-induced G 2 -M arrest was significantly lower in cases than in population controls (1.18 versus 1.44, P < 0.01) and hospital controls (1.18 versus 1.40, P = 0.01). When dichotomized at the 50th percentile value in combined controls (population and hospital controls), a lower level of ;-radiation-induced G 2 -M arrest was associated with an increased risk of lung cancer among African Americans after adjusting for baseline mitotic index, age, gender, and pack-years of smoking [adjusted odd ratio (OR), 2.25; 95% confidence interval (95% CI), 0.97-5.20]. A significant trend of an increased risk of lung cancer with a decreased level of G 2 -M arrest was observed (P trend = 0.02) among African Americans, with a lowest-versus-highest quartile adjusted OR of 3.74 (95% CI, 0.98-14.3). This trend was most apparent among African American females (P trend < 0.01), with a lowest-versushighest quartile adjusted OR of 11.75 (95% CI, 1.47-94.04). The results suggest that a less-efficient DNA damage-induced G 2 -M checkpoint is associated with an increased risk of lung cancer among African Americans. Interestingly, we observed a stronger association of DNA damage-induced G 2 -M arrest and lung cancer among African Americans when compared with Caucasians. If replicated, these results may provide clues to the exceedingly high lung cancer incidence experienced by African Americans. (Cancer Res 2005; 65(20): 9566-73)

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The objective of this study was to estimate the prevalence of self-reported physician-diagnosed systemic lupus erythematosus (SLE) in the USA. During the conduct of an epidemiologic study of systemic sclerosis (scleroderma), 16 607 randomly selected telephone numbers in the continental USA were called to recruit controls. All potentially eligible women were asked 'Have you ever been told by a doctor that you have lupus or SLE'? Of 4034 women aged 18 and above who completed telephone screening, 15 stated they had a physician diagnosis of SLE, corresponding to a prevalence of 372 cases per 100 000 (95% confidence intervals: 208, 614). After review of available medical records in six cases, however, the prevalence of 'validated' SLE was revised to 124 cases per 100 000 (95% confidence intervals: 40, 289). In conclusion, these data suggest that the prevalence of SLE in the USA may be up to three to 10-fold greater than previously estimated. Based on 1990 census data, we would project that over 275 000 women aged 18 and above have SLE in the USA.