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"The results of this study show that α-CbT, a powerful, high-affinity α-7-nAChR inhibitor, induces antitumor activity against NSCLC by triggering apoptosis," wrote Dr. Russo. "The prolonged survival of α-CbT-treated animals in our mouse model of NSCLC is most likely the result of several mechanisms, including various antiproliferative and antiangiogenic effects."

The research also found that unaffected (i.e., noncancerous) cells showed no inhibition of proliferation when treated with α-CbT, suggesting that the treatment would have limited if any toxic effects. Dr. Russo and colleagues postulated that this finding may be due to the reduced number of receptor binding sites on normal cells as opposed to cancerous cells. Conversely, they reported that cancer cells with the greatest number of receptor binding sites seemed to respond with the greatest sensitivity to the treatment.

"The goal of this research line is to explore the widest range of possibilities of intervention on the α7-nAChRs. We hope to move further on towards the clinical setting experimentation phase for the assessment of potentially new treatment strategies for NSCLC," said Dr. Russo.

An editorial in the same issue of the journal asked if nicotine may be to lung cancer what estrogen is to breast cancer. Eliot R. Spindel, M.D., Ph.D., of Oregon Health & Science University, stated that estrogen can stimulate the development of breast cancer and estrogen-receptor antagonists, such as tamoxifen, provide therapeutic benefit. In support of a carcinogenic role for estrogen, the incidence of breast cancer appears to be decreasing as estrogen hormone replacement therapy is being used less often. Likewise, nicotine may
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