Comparative Effectiveness of Radiation Versus Radical Cystectomy for Localized Muscle-Invasive Bladder Cancer

Purpose: Radical cystectomy (RC) with neoadjuvant chemotherapy is the most commonly recommended treatment for muscle-invasive bladder cancer (MIBC), yet RC with urinary diversion remains an invasive treatment. Although some patients with MIBC gain good cancer control with radiation therapy (RT), its effectiveness remains under discussion. Therefore, we aimed to reveal the effectiveness of RT compared with RC for MIBC. Methods and Materials: Using cancer registry and administrative data from 31 hospitals in our prefecture, we recruited patients with bladder cancer (BC) initially registered between January 2013 and December 2015. All patients received RC or RT, and none had metastases. Prognostic factors for overall survival (OS) were analyzed by Cox proportional hazards model and log-rank test. Propensity score matching between the RC and RT groups was performed to examine the association of each factor with OS. Results: Among the patients with BC, 241 received RC and 92 received RT. Median ages of the patients receiving RC and RT were 71.0 and 76.5 years, respectively. Five-year OS rates were 44.8% for patients receiving RC and 27.6% for patients receiving RT (P < .001). Multivariate analysis for OS showed that older age, poorer functional disability, clinical node positive, and pathology of nonurothelial carcinoma were significantly associated with worse prognosis. A propensity score-matching model identified 77 patients with RC and 77 with RT. In this arranged cohort, there were no significant differences in OS between the RC and RT groups (P = .982). Conclusions: Prognostic analysis with matched characteristics showed that patients with BC receiving RT were not significantly different from those receiving RC. These findings could contribute to proper treatment strategies for MIBC

Adipocytes Under Environmental Assault: Targets for Obesity?

Abstract In the recent years, there has been a tremendous concern over the possible health threat posed by endocrine-disrupting chemicals (EDCs). These are mostly synthetic chemicals found in various materials such as organo-chlorinated pesticides, industrial chemicals, plastics and plasticizers, fuels, heavy metals, additives or contaminants in food, and personal care products. These chemicals are present in the environment and are with widespread use. Human exposure to EDCs occurs via ingestion of food, dust and water, via inhalation of gases and particles in the air, and through the skin. Data from several animal models, human clinical observations, and epidemiological studies converge to implicate their association with altered reproductive function in males and females, increased incidence of breast cancer, abnormal growth patterns and neuro-developmental delays in children, disruption of adipocyte function, as well as changes in immune function. The EDCs exert their insulting effects by interfering with hormone biosynthesis, metabolism, or action resulting in a deviation from normal homeostatic control or reproduction. The mechanisms of EDCs involve divergent pathways including (but not limited to) estrogenic, anti-androgenic, thyroid, peroxisome proliferator-activated receptor c, retinoid, and actions through other nuclear receptors; steroidogenic enzymes; neurotransmitter receptors and systems; and many other pathways that are highly conserved in wildlife and humans. Emerging data from in vitro as well as in vivo models suggest new targets (i.e. adipocyte differentiation and mechanisms involved in weight homeostasis) of abnormal programming by EDCs, and provide strong evidence to support the scientific term ‘obesogen’. The emerging idea of a link between EDCs and obesity expands the focus on obesity from intervention and treatment to include prevention and avoidance of these chemical modifiers. Because expansion of the adipocyte pool is critical for safely storing excess lipid, an understanding how these signaling axes can be altered by EDCs is critical in appreciating how environmental contaminants might contribute to the development of metabolic diseases