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Sitaxsentan in pulmonary arterial hypertension.

I am very pleased to comment upon Dr. Daniell’s very scholarly response to our article. His work on prostate cancer and smoking was referenced in our article. I appreciate his bringing to my attention his earlier, related work examining the relationship between smoking and the natural histories of breast and colon cancers. Those studies provide further evidence of an effect of smoking upon the biological behavior of malignancies for which a causal association with smoking has not been established. I agree with Dr. Daniell that systemic effects of smoking, particularly but not limited to immunologic effects, may explain the relationship between smoking and a greater propensity to metastasis. However, I also believe a direct effect of smoking upon the lung to be another, very plausible, contributing factor. In our study, we found that the relationship between smoking and metastatic disease was strongest, in fact, for the subgroup of patients with known metastases limited only to the lung. We have recently validated an animal model of the effects of smoking upon breast cancer metastasis to the lung, and we look forward to employing this model to help clarify the mechanisms involved. As for the issue of hormonal effects of smoking, I agree with Dr. Daniell that, while smoking does have minor hormonal effects, those effects are unlikely to explain the effects of smoking upon metastasis. This possibility was included at the request of the reviewers of the manuscript. In answer to his one specific question about our work, we employed a matched, case-control study design, and axillary lymph node status was one of the factors for which we matched cases and controls. Thus, it is not possible to compare the nodal status for smokers and nonsmokers in our database, which was, by design, the same for both groups.