(American Health Newswire) - New research has indicated that consuming flavonoids - a class of compounds found in fruits, vegetables, dark chocolate and red wine- may indeed lower the risk of stroke in women.

"Studies have shown higher fruit, vegetable and specifically vitamin C intake is associated with reduced stroke risk," Aedín Cassidy, Ph.D., the study's lead author and professor of nutrition at Norwich Medical School in the University of East Anglia in Norwich, United Kingdom, was quoted as saying.

"Flavonoids are thought to provide some of that protection through several mechanisms, including improved blood vessel function and an anti-inflammatory effect."

Cassidy and colleagues used 14-years of follow-up data from the Nurse's Health Study, which included 69,622 women who reported their food intake, including details on fruit and vegetable consumption every four years. Researchers examined the relationship of the six main subclasses of flavonoids commonly consumed in the U.S. diet: flavanones, anthocyanins, flavan-3-ols, flavonoid polymers, flavonols and flavones with risk of ischemic, hemorrhagic and total stroke.

As expected, the researchers didn't find a beneficial association between total flavonoid consumption and stroke risk, as the biological activity of the sub-classes differ. However, they found that women who ate high amounts of flavanones in citrus had a 19 percent lower risk of blood clot-related (ischemic) stroke than women who consumed the least amounts.

In the study, flavanones came primarily from oranges and orange juice (82 percent) and grapefruit and grapefruit juice (14 percent). However, researchers recommended that consumers increase their citrus fruit intake, rather than juice, due to the high sugar content of commercial fruit juices.

More studies are needed to confirm the association between flavanone consumption and stroke risk, and to gain a better understanding about why the association occurs, the authors said.

SOURCE: American Heart Association, February  2012

(American Health Newswire) - Researchers have discovered how a protein "master regulator" goes awry, leading to metastasis, the fatal step of cancer.

The protein mTOR is a "master regulator" of human protein synthesis. It helps normal cells sense nutrients and control cell growth and metabolism. But in many forms of cancer, this process goes awry, and mTOR reprograms normal cells to aberrantly divide, invade and metastasize.

In the human body, mTOR is a molecular sensor that helps cells respond to favorable or unfavorable environments. Under ordinary conditions, it acts as a master regulator of genes that induce cells to growth and divide. In times of scarcity, when somebody is starving for instance, mTOR shuts down much of the machinery that makes proteins so that an organism can conserve energy.

"We are now discovering that during tumor formation mTOR leads to metastasis by altering the synthesis of a specific group of proteins that make the cancer cells move and invade normal organs," Davide Ruggero, PhD, an associate professor of urology and member of the Helen Diller Family Comprehensive Cancer Center and the Multiple Myeloma Translational Initiative at UCSF, was quoted as saying.

In their research, Ruggero and his colleagues suggests why drugs like Rapamycin-a drug used to block mTOR- have failed.

"The problem," said Ruggero, "is that they block mTOR, but not completely."

When drugs like Rapamycin fail to completely stop mTOR from working, they allow it to continue pushing a cancer cell toward malignancy. Some newer compounds that block mTOR do so more completely, and the team led by Ruggero showed in preclinical experiments that this effectively hobbles the cancer cells.

In their research, Ruggero and his colleagues showed that a mouse model of human prostate cancer treated with a new experimental drug called INK128 did not metastasize. They also showed that the new drug has a strong therapeutic effect on human prostate cancer cells.

"While the experiments were primarily focused in prostate cancer, we believe this work is widely applicable in many tumor types because mTOR is a critical regulator of so many cancers," author Andrew Hsieh, MD, a clinical oncologist in the UCSF Department of Medicine, Division of Hematology/Oncology and a senior member of the Ruggero laboratory, was quoted as saying.

"For example, clinicians Jeff Wolf and Tom Martin are now testing INK128 here at UCSF, in multiple myeloma patients," Ruggero said.

The research also found that INK128 works better by also restraining abnormal protein synthesis when mTOR is hyperactive. "Deregulations in protein synthesis is now becoming a hallmark of cancer, and we are very excited by the opportunity to target the aberrant protein synthesis apparatus in many cancers," Ruggero said.

SOURCE: The Journal Nature, February  2012