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Troglitazone (TRO) and rosiglitazone (RSG) belong to the thiazolidinedione class (insulin-sensitizing agents) and exert many of their metabolic effects as peroxisome proliferator-activated receptor gamma (PPARgamma) ligands. In the present study we examined the effects of TRO and RSG on LDL-induced VSMC growth. Pretreatment of VSMC with 1 microM TRO or 0.1 microM RSG completely blocked the LDL-induced cell proliferation as measured by [3H]thymidine incorporation into DNA and by determination of the cell number. We then examined with Western blotting whether these growth suppressing effects are mediated through the mitogen-activated protein kinase (MAPK) pathway, a common signaling pathway activated by growth factors. TRO and RSG had no effect on the LDL-induced stimulation of the MAP kinases ERK1/2, p38 and SAP/JNK. We conclude that thiazolidinediones are potent inhibitors of LDL-induced VSMC growth acting downstream of the cytoplasmic activation of MAPK.

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In a Yugoslav village, psychosocial, anamnestic medical, and pathophysiological data were recorded for 1,353 persons in a longitudinal study. The role of psychosocial stress in carcinogenesis, as far as we have investigated it, may be described as follows: (1) Psychosocial stress in terms of high hopelessness, high antiemotionality, etc. has a strong relevance for cancer incidence which does not act via one of our physiological variables associated with cancer. This follows from the results of our multivariate analysis. (2) Psychosocial stress is substantially associated with a low lymphocyte percentage, which in turn is a relatively strong risk factor for cancer. (3) Psychosocial stress is relatively weakly associated with the cholesterol minimum; but apart from the fact that the cholesterol characteristics of cancer subjects are more marked descriptively under stress conditions, psychosocial stress significantly enhances the efficacy of the most important physiological risk variables for cancer.

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