Purpose: A role for estrogens in determining lung cancer risk and prognosis is suggested by reported sex differences in susceptibility and survival. Archival lung tissue was evaluated for the presence of nuclear estrogen receptor (ER)-a and ER-h and the relationship between ER status, subject characteristics, and survival. Experimental Design: Paraffin-embedded lung tumor samples were obtained from 214 women and 64 men from two population-based, case-control studies as were 10 normal lung autopsy samples from patients without cancer. Nuclear ER-a and ER-h expression was determined by immunohistochemistry. Logistic regression was used to identify factors associated with ER positivity and Cox proportional hazards models were used to measure survival differences by ER status. Results: Neither tumor (0 of 94) nor normal (0 of 10) lung tissue stained positive for ER-a. Nuclear ER-h positivity was present in 61% of tumor tissue samples (170 of 278; 70.3% in men and 58.3% in women) and 20% of normal tissue samples (2 of 10; P = 0.01). In multivariate analyses, females were 46% less likely to have ER-h^positive tumors than males (odds ratio, 0.54; 95% confidence interval, 0.27-1.08). This relationship was stronger and statistically significant in adenocarcinomas (odds ratio, 0.40; 95% confidence interval, 0.18-0.89). Women with ERh^positive tumors had a nonsignificant 73% (P = 0.1) increase in mortality, whereas men with ER-h^positive tumors had a significant 55% (P = 0.04) reduction in mortality compared with those with ER-h^negative tumors. Conclusions: This study suggests differential expression by sex and influence on survival in men of nuclear ER-h in lung cancer, particularly in adenocarcinomas.In the United States, lung cancer is the second most common cancer among both men and women and is the leading cause of cancer death in both sexes (1). A number of studies report that women are more susceptible, dose for dose, to the carcinogenic effects of cigarette smoke than men (2, 3). Women have been reported to have higher levels of polycyclic aromatic hydrocarbon-DNA adducts than men at any given level of smoking (4). Smoking females have significantly higher levels of expression of the gene encoding CYP1A1, a central enzyme in the metabolic activation of polycyclic aromatic hydrocarbons (4, 5). It has also been shown that G:C to T:A transversions in p53 are more common among females with lung cancer than males (6). One study also reported that the proportion of nonsmoking lung cancer cases in women was double that in men, suggesting that even nonsmoking women may be more susceptible to lung carcinogens than nonsmoking men (2).The reported sex difference in susceptibility suggests a role for hormones in determining lung cancer risk. Both exogenous estrogens [i.e., hormone replacement therapy (HRT) and oral contraceptives] and endogenous hormone levels (i.e., age at menopause) may contribute to the development of lung cancer (7 -10). Early age at menopause has been associated with decreased risk of adenocarci...

These findings suggest that postmenopausal hormone exposures are associated with reduced risk of ER-alpha- and ER-beta-expressing NSCLC. Understanding tumor characteristics may direct development of targeted treatment for this disease.

Background In this study we assessed patient outcomes after complete endoscopic sinus surgery (ESS) and aspirin desensitization for patients with aspirin‐exacerbated respiratory disease (AERD). Methods A retrospective chart review was conducted for patients with aspirin challenge–proven AERD who underwent complete ESS followed by aspirin desensitization. Outcomes assessed included need for revision surgery and quality‐of‐life measures using the 22‐item Sino‐Nasal Outcomes Test (SNOT‐22). Data were collected preoperatively, postoperatively prior to desensitization, and then at intervals post‐desensitization through 30 months after aspirin desensitization. A longitudinal linear mixed‐effects model was used for data analysis. Results Thirty‐four patients met the inclusion criteria for this study. Thirty‐two patients successfully completed aspirin desensitization and were subsequently followed for 30 months after desensitization. Two patients were unable to complete desensitization. Five patients discontinued aspirin maintenance therapy due to gastrointestinal and respiratory side effects. Within the follow‐up period, there were only 3 (9.4%) revision sinus surgeries. Notably, 1 of these revision cases occurred in a patient who had discontinued aspirin maintenance therapy. After surgical treatment and prior to desensitization patients had significant reductions in SNOT‐22 scores. Our results demonstrate that total SNOT‐22 scores remained statistically unchanged from immediate post‐desensitization throughout the 30‐month follow‐up period. Conclusion Complete sinus surgery followed by timely aspirin desensitization and maintenance therapy is an effective combination in the long‐term management of sinus disease in patients with AERD.