Cancer prevention: stopping cancer before it can start

All mice had temporary tumor regression in the absence of androgen, but then the untreated mice experienced substantial tumor regrowth as the tumor become androgen-independent. Mice treated with a single drug had some reduction of androgen-independent tumor growth, while administration of atorvastatin and celecoxib in combination resulted in a more potent inhibition of androgen-independent growth than either drug alone. “The agents appear to work by inhibiting a signal transduction pathway that is important for the growth of these cancer cells,” Zheng said.

Although a high dose of celecoxib has been linked to a small increase in cardiovascular risk in prior human studies, Zheng said the dose used in this study was low and the benefits should outweigh the risks.

Dietary energy balance impacts spontaneous pancreatic lesions in the K5.COX-2 transgenic model of pancreatic cancer: Abstract 4188

Shedding light on the links between obesity and cancer, researchers at the University of Texas M. D. Anderson Cancer Center report that modulating energy balance by restricting calories can prevent pancreatic cancer in laboratory models.

“We are very excited that our research may lead to insights to prevent or control this deadly disease in the near future,” said lead researcher Laura M. Lashinger, Ph.D., a post-doctoral fellow at M. D. Anderson.

Pancreatic cancer is the fourth leading cause of cancer death in both men and women in the United States. Obesity, the overall rate of which has risen sharply over the past 40 years, has emerged in epidemiological studies as a key risk factor for pancreatic cancer.

Other studies have shown that calorie restriction, a dietary strategy for inducing negative energy balance and preventing or reversing obesity, has significant anticancer effects in several species, against a variety of tumor types. However, the exact mechanisms underlying the obesity-pancreatic cancer association are not clearly understood.

“It is likely that inflammation may be playing a role,” Lashinger said. “Fat tissue is more than simply weight; it produces an inflammatory property that leads to greater risk of cancer and other diseases.”

In the current study, Lashinger and colleagues hypothesized that spontaneous tumor development in the K5.COX-2 transgenic mouse model of pancreatitis-driven pancreatic cancer would be reduced in lean mice, when compared with overweight or diet-induced obese mice.

They placed 36 mice on one of three diets for 14 weeks: a lean diet with a 30 percent calorie restriction (n = 12), an overweight diet (n = 12), or a high calorie, high fat diet–induced obese regimen (n = 12).