Cromolyn Halts Pancreatic Cancer in Mice
In murine model, cromolyn stopped tumor growth and increased gemcitabine's efficacy
TUESDAY, Dec. 26 (HealthDay News) -- By binding with S100P, a protein expressed in 90 percent of pancreatic cancers, cromolyn blocks the receptor for advanced glycation end-products (RAGE) activation, thereby inhibiting tumor growth and enhancing the efficacy of gemcitabine, the drug used to treat pancreatic cancer. The experimental research is published in the Dec. 20 issue of the Journal of the National Cancer Institute.
Thiruvengadam Arumugam, Ph.D., of the University of Texas M.D. Anderson Cancer Center in Houston, and colleagues investigated cromolyn's effect on S100P and RAGE in in vitro and in vivo murine pancreatic cancer models. Tumor growth was assessed with reporter gene expression in the in vivo studies. Three orthotopic models (20 mice per model) were used in which cromolyn was given with and without gemcitabine.
In vitro studies showed that, compared to controls, cromolyn significantly blocked S100P and RAGE co-immunoprecipitation. The results were confirmed with in vivo studies that demonstrated cromolyn significantly inhibited growth in tumors with endogenous S100P and significantly enhanced gemcitabine's efficacy, compared to controls.
"Cromolyn treatment in combination with gemcitabine should be tested to improve patient outcome with this deadly aggressive cancer. Whether cromolyn may also improve responses to cytotoxic treatments in other cancers would also appear to be worth further investigation," the authors conclude.