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Vol. LXIII, No. 3
February 4, 2011
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Digest

Study Uncovers Pathway Critical for UV-Induced Melanoma

Scientists have made an unanticipated discovery in mice that interferon-gamma, a type of protein primarily used by the immune system for intercellular communication, acts as a promoter for the deadly form of skin cancer known as melanoma. This finding resulted from a series of experiments designed to understand how solar ultraviolet (UV) radiation causes melanoma.

Results of this study suggest that interferon-gamma, which has been thought to contribute to an innate defense system against cancer, under some circumstances may promote melanoma and incite the development of tumors. The work, led by Dr. Glenn Merlino of NCI’s Laboratory of Cancer Biology and Genetics and research fellow and first author Dr. M. Raza Zaidi, appeared online Jan. 19 in Nature. Cutaneous melanoma is a highly aggressive and frequently drug-resistant cancer with rising incidence rates. The major environmental risk factor for melanoma is UV radiation exposure, usually from the sun, with the highest risk associated with intermittent burning doses, especially during childhood.

Over the past 10 years, the researchers used genetically engineered mice first to prove, and then to try to understand, the connection between exposure to UV radiation and the initiation of melanoma. The current work was the latest attempt to define the molecular mechanisms of this cause and effect relationship. The results of this study offer the possibility that the inhibition of interferon-gamma immediately after sunburn might block the carcinogenic activation of the skin’s pigment-producing cells, known as melanocytes, making it a potentially effective preventive strategy against UV radiation-induced melanoma, according to the scientists.

Rebooting the Brain Helps Stop the Ring of Tinnitus

The hallmark of tinnitus is often a persistent ringing in the ears that is annoying for some, debilitating for others and currently incurable. Similar to pressing a reset button in the brain, the new therapy was found to help retrain the part of the brain that interprets sound so that errant neurons reverted back to their original state and the ringing disappeared.

The hallmark of tinnitus is often a persistent ringing in the ears that is annoying for some, debilitating for others and currently incurable. Similar to pressing a reset button in the brain, the new therapy was found to help retrain the part of the brain that interprets sound so that errant neurons reverted back to their original state and the ringing disappeared.

NIH-funded researchers were able to eliminate tinnitus in a group of rats by stimulating a nerve in the neck while simultaneously playing a variety of sound tones over an extended period of time, says a study published Jan. 12 in the advance online edition of Nature. The hallmark of tinnitus is often a persistent ringing in the ears that is annoying for some, debilitating for others and currently incurable. Similar to pressing a reset button in the brain, this new therapy was found to help retrain the part of the brain that interprets sound so that errant neurons reverted back to their original state and the ringing disappeared. The research was conducted by scientists from the University of Texas at Dallas and MicroTransponder Inc. NIDCD funded a large part of the research.

Tinnitus is a symptom some people experience as a result of hearing loss. When sensory cells in the inner ear are damaged, such as from loud noise, the resulting hearing loss changes some of the signals sent from the ear to the brain. For reasons that are not fully understood, some people will develop tinnitus as a result.

New Technology Peeks Deep into the Brain

Changes within deep regions of the brain can now be visualized at the cellular level, based on NIH-funded research on mice. Published online in the Jan. 16 Nature Medicine, the study used a groundbreaking technique to explore cellular-level changes over a period of weeks within deep brain regions, providing a level of detail not possible with previously available methods. NIDA, NCI and NINDS supported the study. Researchers at Stanford University used time-lapse fluorescence microendoscopy, a technique that uses miniature probes to directly visualize specific cells over a period of time, to explore structural changes that occur in neurons as a result of tumor formation and increased stimulation in the mouse brain. This could lead to greater information on how the brain adapts to changing situations, including repeated drug exposure.

“Continued drug use leads to changes in neuronal circuits that are evident well after a person stops taking an addictive substance,” said NIDA director Dr. Nora Volkow. “This study demonstrates an innovative technique that allows for a glimpse of these cellular changes within the brain regions implicated in drug reward, providing an important tool in our understanding and treatment of addiction.”—


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