Polymorphisms of CYP19A1 may be related to the increased risk of lung cancer; in particular, haplotype ACA may contribute to lung-cancer progression in nonsmokers.
This review discusses the recent literature findings about the biology of the ERs, aromatase, and the progesterone receptor in lung cancer and highlights the ongoing clinical trials and future therapeutic implications of these findings.
Breast cancer survivors can offer a unique patient cohort to examine the effect of antiestrogen therapy on lung cancer carcinogenesis because many of these women would have received long-term selective estrogen receptor modulators (SERMs) and/or aromatase inhibitors (AIs) as adjuvant treatment.
We previously showed that the aromatase inhibitor (AI) anastrozole decreased development of tobacco carcinogen-induced lung tumors in a murine lung cancer prevention model and that aromatase and estrogen receptor were expressed in pulmonary inflammatory cells.