Differences in Functional Capacity between Oncologic and Non-Oncologic Populations: Reference Values.

This study is focused on the fact that in the context of increasing global aging and cancer diagnoses, additional challenges arise in clinical care. Adequate functionality and body composition are key to coping with antineoplastic treatment, which can lead to better treatment tolerance, survival, and quality of life. This is a cross-sectional comparative study focused on the assessment and comparison of body composition and functionality between cancer patients and a reference population, with the aim of establishing meaningful baseline values. Techniques such as manual dynamometry, the Five-Times Sit-to-Stand test, and bioimpedance were used to collect data from 374 oncologic patients and 1244 reference individuals. The results reveal significant disparities in functionality and body composition among participants, and provide age group-specific adjusted baseline values for those diagnosed with cancer. These findings may have crucial clinical implications for applying particular cut-off points designed for this population group, which makes the assessment process faster and more accurate, enhances the capacity of medical personnel to act quickly, and improves the management of frailty in cancer patients.

Proangiogenic role of tumor-activated hepatic stellate cells in experimental melanoma metastasis.

Myofibroblasts infiltrate malignant liver tumors, although their pathogenic implications are unclear. Immunohistochemical detection of alpha-smooth muscle actin, glial fibrillary acidic protein (GFAP), and CD31 and CD34 expression was used to analyze the contribution of myofibroblasts to angiogenesis in hepatic metastasis produced by intrasplenically-injected B16 melanoma (B16M). Because activated hepatic stellate cells (HSCs) are oxygen-sensing myofibroblasts producing vascular endothelial growth factor (VEGF), the effect of B16M and human A375 melanoma supernatants on VEGF production by immortalized rat HSC line T6 and primary cultured human HSCs also was studied under an hypoxic atmosphere mimicking a tumor microenvironment. Myofibroblast infiltration preceded endothelium recruitment in avascular micrometastasis and generated specific stroma for sinusoidal-type and portal-type angiogeneses. Thereafter, myofibroblasts and endothelial cells colocalized within both angiogenic patterns and their numerical densities correlated with metastasis development. Myofibroblasts often were GFAP-positive, suggesting an HSC origin. Melanoma supernatants stimulated VEGF messenger RNA and protein synthesis by HSCs. These effects were potentiated by hypoxia. VEGF up-regulation was accompanied by increased expression of cyclooxygenase type 2 (COX-2) and PGE2 synthesis. HSC production of VEGF decreased under COX-2 inhibition, whereas it was increased by exogenous PGE2. The high VEGF expression in HSCs induced by melanoma factors and hypoxia resulted in mitogenic, antiapoptotic, and motogenic stimulation of both murine hepatic sinusoidal endothelium and human umbilical vein endothelium. In conclusion, temporal and positional relationships evolve between myofibroblast and endothelium recruitment during metastasis development. Mechanistically, hypoxic induction of VEGF in tumor-activated HSCs may create a proangiogenic microenvironment, facilitating endothelial cell recruitment and survival during hepatic metastasis transition from an avascular to a vascular stage.