Key Role of Obesity in Genitourinary Tumors with Emphasis on Urothelial and Prostate Cancers.

摘要: Background: In human populations, a certain amount of data correlate obesity/body mass index (BMI) with urothelial cancer (UC) and prostate (PCa) occurrence, however this is not fully elucidated at all stages disease. an attempt to shed light on uncertain areas in such field, the present review we illustrate main molecular mechanisms linking obesity cancer, focusing correlation between tumor risk, disease progression response chemo- immunotherapy patients UC predictive/prognostic role PCa treated currently available therapeutic approaches. Methods: We did large-scale literature search existing scientific websites keywords “obesity”, “body (BMI)”, “urothelial cancer”, “prostate “docetaxel”, “cabazitaxel”, “abiraterone acetate”, “enzalutamide”, “radium223”. Results: Many adipocytes-induced molecules support proliferation through activation various cellular pathways. The evidence postoperative setting do BMI oncological outcomes prediction still completely clear. Likewise, metastatic controversial results link obesity/BMI clinical chemotherapy. Adipose stromal cells recruitment, induced by cells, from white adipose tissue sites inducing cell invasiveness was associated poor survival. Conflicting data, although more oriented towards better survival outcome, resulted obese docetaxel. cell-lines cabazitaxel chemo resistance (ASC)-mediated demonstrated. castration-resistant high (>25 kg/m2) receiving abiraterone acetate there were significant worse outcomes, while enzalutamide affect outcome. radium 223 higher significantly correlated favorable overall Conclusions: focus understand interplay UC/PCa. Several pathogenic pathways exploring issue are discussed, opening way challenging tailored treatments basis BMI. Improving knowledge connections could favor development new therapies likely reducing drug resistance.