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GeneAlert ... from UPI

By PEGGY PECK, United Press International

TWIST EXPLAINS WHY SOME CANCERS SPREAD

A new study shows tumors metastasize by reactivating a "sleeper" protein that should have been shut off permanently. A team of Whitehead researchers discovered breast carcinomas in mice hijack a gene regulator protein called Twist, which should have become dormant after early embryonic development. Twist allows cancer cells to spread throughout the body, or metastasize. The researchers made the discovery by comparing metastatic and non-metastatic cancer cells taken from mouse tumors. Using microarray technology, they found certain genes were active only in the metastatic tumors -- and the gene coding for the protein Twist stood out from all others. When the Twist gene was disabled, mice developed primary, localized breast tumors, but the tumors were unable to metastasize. The results of this research are published in the June 25 issue of Cell.

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'MIGHTY MOUSE' GENE ALSO WORKS IN PEOPLE

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The silencing of a gene that makes mice twice as muscular has the same affect in humans, researchers found. An international team made up of German scientists and researchers from Johns Hopkins University in Baltimore made the discovery while studying the genes of a German boy who was born with unusually large muscles. The child's muscularity was caused by an inherited mutation that effectively silenced the myostatin gene, a condition previously tied to the development of super muscular mice or "mighty mice." Body-builders and people suffering from muscle-wasting diseases like muscular dystrophy have been closely following the work on myostatin, hoping that what worked in mice also would work in people. Researchers said the finding gives hope that agents that block myostatin activity in mice may be able to increase muscle mass in humans. The study appeared in the June 24 issue of the New England Journal of Medicine.


GENE VARIANT LINKED TO PARKINSON'S DISEASE RISK

A form of the APOE gene that is protective in Alzheimer's disease appears to slightly increase risk for Parkinson's disease. Researchers from the University of North Carolina at Chapel Hill combined the results of 22 studies to learn more about the role of the APOE gene in Parkinson's. APOE-4 has been linked with an increased risk for Alzheimer's disease, while APOE-2 occurred less frequently in people with Alzheimer's. As a result, APOE-4 was thought to be the "bad guy" while APOE-2 was the "good guy." This new study may change the image of APOE-2. "We found that APOE-2 conveyed a slight but statistically significant risk for Parkinson's disease, with an odds ration of 1.2," said one researcher. "This means that people with this gene have about a 20 percent higher chance of developing Parkinson's disease than people without it." The study did not find any link between APOE-4 and Parkinson's disease. The study was published this week in the June issue of Neurology.

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GENE EXPRESSION IN LIVING COLOR

A new imaging technology allows scientists to get a picture of gene expression in living mice. Case Western Reserve University researchers treated mice with genetic material that should theoretically correct the defect that causes cystic fibrosis. Then, using the radioactive tracer iodine-125 FIAU and a custom-built small animal imaging system that combines X-ray and planar gamma scintigraphy, the team showed the genetic material was being expressed in the lungs of the mice, right where it needed to be. "Though the results are preliminary, they are extremely encouraging," according to one scientist. The researchers will continue to test their mice model systems, and work to translate the technology to human patients after their preliminary studies are completed. The research was presented at the 51st Annual Meeting of the Society of Nuclear Medicine on June 21.


A NOVEL METHOD FOR INTRODUCING TRANSGENES

Transgenic material has been carried directly into offspring using sperm stem cells "infected" by a retrovirus. Reproductive biologists from Kyoto University in Japan injected the retrovirus into the seminiferous tubules in the testes of immature male mice, which caused the retrovirus to be taken up by the sperm stem cells, producing sperm with the transgene. Eighty-six percent of the mice injected with the retrovirus became fertile, and 26 percent of these males later mated with wild-type female mice and sired offspring. An average of about 3 percent of these offspring had the transgene. The Japanese team noted other methods have been described for introducing transgenes into animals, including techniques based on eggs or embryos from female animals, but the success rate for these methods is generally less than 1 percent. The researchers said the new transgenic reproductive method should be directly applicable for producing a wide range of animals. The research was released June 21, and has been accepted for publication in the journal Biology of Reproduction.

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(EDITORS: For TWIST, contact David Cameron at (617) 258-5183 or [email protected]. For MIGHTY, contact Joanna Downer at (410) 614-5105 or [email protected]. For VARIANT, contact Dr. Xuemei Huang at (919) 843-4143 or [email protected]. For GENE EXPRESSION, contact Darren DiPatri at (202) 955-1242 or [email protected]. For NOVEL, contact Dr. Takashi Shinohara at 81-75-753-9306 or [email protected])

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