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The role of parathyroid hormone-related peptide (PTHrP) in the regulation of hypercalcemia in patients with malignancies is well studied, but whether its expression in tumor tissue correlates with tumor progression is not clear at present. The majority of tumors that metastasize to the bone produce PTHrP, and PTHrP expression correlates with skeletal localization of tumors. About 95% of colorectal adenocarcinomas overexpress PTHrP mRNA and protein, and the expression level is higher in poorly differentiated than in well-differentiated adenocarcinomas. However, there is some controversy at present about the prognostic significance of PTHrP expression on primary tumor cells, and studies suggest that there might be tissue-specific responses. We will briefly present here existing evidences that suggest that the expression of PTHrP in the primary tumor tissue could have both positive and/or negative impact on tumor progression and clinical outcome of the disease.

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Prolonged hypertension causes structural changes including glomerulosclerosis and tubulointerstitial damage of the kidney, termed benign nephrosclerosis. It is generally accepted that, in benign nephrosclerosis, increased accumulation of extracellular matrix in the glomeruli results in glomerulosclerosis. Little is known, however, about the possible role of the extracellular matrix in the tubulointerstitial damage in benign nephrosclerosis. In this study, the possible roles of type IV basement-membrane collagen and type III interstitial collagen in tubulointerstitial damage caused by hypertension were explored. Immunohistochemical techniques were used to investigate the distribution of type III and type IV collagens in the kidney sections of 15 patients with benign nephrosclerosis with tubulointerstitial damage and in 10 controls. In the control renal sections strong immunostaining for type III collagen was found in the interstitium and immunostaining for type IV collagen was present in the tubular basement membrane and weakly in the interstitium. In the patients with tubulointerstitial damage there was increased immunostaining for both type III and type IV collagens in the expanded interstitium and damaged tubules than was found in the control kidney sections. These findings indicate that increased accumulation of both type III and type IV collagens might play a significant role in the tubulointerstitial damage in benign nephrosclerosis.

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