egression, 15 of the 17 underwent surgery, achieving local control. All 5 with inflammatory Ca had elimination of the inflammatory component. A variety of combinations are available for recurrent or metastatic disease, but there are few prospective trials which compare the various treatment regimens and stratify for the prognostic variables. This program randomly compares 3 active regimens for response rates and duration of survival, and evaluates the effect of MER immunotherapy. A group effort is necessary to stratify for the variables. Interim evaluations of the 335 pts entered show that prior postoperative adjuvant radiotherapy is a detrimental factor for determining response. MER immunotherapy also had a detrimental effect upon response rate (p equals .003) and survival was shorter. Further randomization to MER has been discontinued. Interim evaluations of the treatment arms revealed slight but not significant differences among the chemotherapy regimens.

Obesity is a world-wide health problem that is associated with metabolic syndrome, including insulin resistance and the development of non-alcoholic fatty liver disease (NAFLD). NAFLD is characterized by hepatic steatosis and varying degrees of inflammation and fibrosis. Increasing evidence suggests that saturated free fatty acids (FFA), by promoting insulin resistance and mediating the progression from simple steatosis to steatohepatitis, are a causative link between obesity and NAFLD. However, the molecular mechanisms responsible for the effects of saturated FFA are incompletely understood. Our long-term goal is to understand the molecular mechanisms by which saturated FFA contribute to the development of NAFLD. Saturated FFA are a major source of metabolic stress that induce activation of the c-Jun NH2-terminal kinase (JNK) pathway, and gene deletion and pharmacological inhibition have established an important role for the JNK signaling pathway in obesity-induced insulin resistance and the pathogenesis of NAFLD. Our preliminary studies identified the MAP3