TGF-βs as candidate biomarkers
One major goal in the field of prevention is the identification of surrogate biomarkers that might rapidly predict the effect of a given agent on the primary end-point of cancer incidence. There is an extensive literature showing that steroid hormone superfamily members, such as antiestrogens and retinoids, can upregulate TGF-β activity in a variety of systems [12,13,14,15,16,17,23,24,35]. This suggested that the chemopreventive action of these agents against breast cancer could be mediated in part through enhancing the tumor suppressor activity of the endogenous TGF-β system, and thus that changes in TGF-β expression might serve as useful surrogate end-point biomarkers of chemopreventive efficacy. However, here we used the NMU-induced rat model of mammary carcinogenesis to show that the chemopreventive effect of tamoxifen and two retinoids is not associated with any consistent changes in TGF-β levels, at least as determined immunohistochemically.