山口 博紀

Although the proportion of early gastric cancer is rising in the incidence of gastric cancer as a whole, its natural, history is still under discussion. We report a patient who was diagnosed with early gastric cancer and who had undergonebarium studies once a year for the three previous years.The exact, increasing size of the tumour could be measured at these four time points, and the data show, almost exactly, the line calculated by the formula S=0.3t(2) [S= size (cm(2)) of the cancerous lesion, t=time (yr) elapsed from the beginning of the gartric cancer].

Purpose. In the present study, we investigated the effect of troglitazone, a selective ligand and agonist of PPAR-gamma on the metastatic potential of human colon cancer cells. Methods. High- and low-PPAR-gamma expression clones of the colon cancer cell line, HT29, namely clones 21 and 3 respectively, were used. We investigated the effect of troglitazone on the proliferation, on the adhesion to extracellular matrix proteins and on the synthesis of matrix metalloproteinases (MMPs) of colon cancer cells. Results. Troglitazone inhibited the proliferation of both subclones, in a dose-dependent manner, and the inhibitory effect correlated with the level of PPAR-gamma expression. Troglitazone strongly inhibited the production of MMP-7, an enzyme associated with invasiveness of cancer cells, by both subclones. In addition, troglitazone caused a strong decrease in the adhesion of clone 21 to extracellular matrix (ECM) proteins, laminin and type IV collagen. This effect was independent of beta1-integrins expression. Conclusion. In addition to inhibition of cancer cell growth, troglitazone had an inhibitory effect on two important events associated with the metastatic potential of cancer cells, production of MMPs and adhesion to ECM proteins. Consequently, troglitazone is a promising agent for the treatment and prevention of colon cancer metastasis.