Bach reported that he has received speaking fees from Genentech. Dr. Detterbeck reported that he was reimbursed for travel costs associated with his work on the Oncimmune advisory board, and has participated without compensation in a symposium on CT screening sponsored by Covidien. Dr.Berry reported that he is co-owner of Berry Consultants LLC which designs adaptive clinical trials for pharmaceutical companies, medical device companies and NIH cooperative groups. To the best of his knowledge none of these parties have any interest in lung cancer screening. Dr. Gould reported that he receives grant support from the National Cancer Institute. Dr. Jett reported that he has grants pending for work related to screening and early detection of lung cancer with Oncimmune and Isense. Dr. Sabichi reported her membership on the National Cancer Institute's PDQ Prevention and Screening Editorial Board and her possession of a pending patent for a test for the detection of bladder cancer. Dr. Wood reported his participation in the development of the National Comprehensive Cancer Network's clinical practice guidelines for lung cancer screening in his role as Chair of the NCCN Lung Cancer Screening Panel.

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We have previously demonstrated decreased Jun/AP-1 activity in the breast cancer cell line MCF-7 when compared to normal or immortalized mammary epithelial cells. In this paper, we overexpress Jun in MCF-7 cells (MCF7Jun) and demonstrate that it results in diverse biologic and biochemical changes, which mimic those seen clinically in breast cancer. Overexpression of Jun causes signi®cant alterations in the composition of AP-1, decreased junB and increased fra-1 expression and results in an increased biologic aggressiveness. MCF7Jun cells exhibit increased cellular motility, increased expression of a matrix degrading enzyme MMP-9, increased in vitro chemoinvasion and tumor formation in nude mice in the absence of exogenous estrogens. Furthermore, MCF7Jun cells are unresponsive to the growth stimulating e ects of estrogen and growth inhibitory e ects of tamoxifen. Analysis of the estrogen receptor (ER) expression and activity showed that the MCF7Jun cells have no detectable ER. MCF-7 cells overexpressing mutant forms of cJun were responsive to the growth stimulatory e ects of estrogen indicating that full-length cJun is required to acquire the estrogenindependent phenotype in breast cancer cells.