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LOS ANGELES, July 18 (Xinhua) -- At least 70 genetic mutations may be involved in the formation of colon cancer, far more than scientists previously thought, a new study suggests.The study by researchers at University of Texas (UT) Southwestern Medical Center contradicts previous thinking that only a few mutated genes may play a role in the development of colon cancer."The ways we've been treating patients up to now is to just go after one target when we should be going after three to four different pathways simultaneously," said Dr. Jerry W. Shay, vice chairman and professor of cell biology at UT Southwestern.The new study identified 65 candidate genes and at least five passenger genes whose mutations play significant roles in cancer development. Inactivating the function of any of these tumor- suppressing genes led to a key step in cancer development called anchorage-independent growth, meaning cells piled up on top of each other rather than aligning neatly.According to previous studies, there were 151 candidate genes and that mutations in just eight to 15 of them would lead to cancer. There were 700 other genes classified as passenger genes whose mutations were incidental to cancer growth.Current cancer treatments target just one or two known cancer- driver genes. While patients may get transient tumor burden reduction, almost universally tumor growth returns."Those numbers are dead wrong," Dr. Shay said, suggesting a new approach to colon cancer treatments targeting multiple genes and pathways simultaneously.The next step is further research to classify more accurately which genes drive cancer and which are merely passengers, the researchers said.Study findings were published in the July 2011 Cancer Research (Priority Reports).
LOS ANGELES, July 18 (Xinhua) -- U.S. scientists have proven that oncogenes can change normal cells into stem-like cells, paving the way to a safer and more practical approach to treating diseases like multiple sclerosis and cancer with stem cell therapy.In a collaborative study, researchers from the Keck School of Medicine of the University of Southern California (USC), and the Children's Hospital of Orange County (CHOC) in California and Good Samaritan Hospital Medical Center in New York have successfully converted human skin cells into brain cells by suppressing the expression of p53, a protein encoded by a widely studied oncogene. This suggests that p53 mutation helps determine cell fate -- good or bad -- rather than only the outcome of cancer.Oncogenes are generally thought to be genes that, when mutated, change healthy cells into cancerous tumor cells.Study findings were appearing Monday on the website of the American Association for the Advancement of Science (AAAS)."The reality may be more complicated than people think," said Jiang F. Zhong, Ph.D., assistant professor of pathology at the Keck School. "What is a stem cell gene? What is a cancer gene? It may be the same thing.""When you turn off p53, people think the cell becomes cancerous because we tend to focus on the bad thing," Zhong said. "Actually, the cell becomes more plastic and could do good things, too. Let's say the cell is like a person who loses his job (the restriction of p53). He could become a criminal or he could find another job and have a positive effect on society. What pushes him one way or the other, we don't know because the environment is very complicated."Stem cells can divide and differentiate into different types of cells in the body. In humans, embryonic stem cells differentiate into three families, or germ layers, of cells. The reasons why and how certain stem cells differentiate into particular layers are not clearly understood. However, from those layers, tissues and organs develop. The endoderm, for example, leads to formation of the stomach, colon and lungs, while the mesoderm forms blood, bone and heart tissue. In its study, Zhong's team examined human skin cells, which are related to brain and neural cells from the ectoderm.When p53 was suppressed, the skin cells developed into cells that looked exactly like human embryonic stem cells. But, unlike other man-made stem cells that are "pluripotent" and can become any other cells in the body, these cells differentiated only into cells from the same germ layer, ectoderm."IPSCs (induced pluripotent stem cells) can turn into anything, so they are hard to control," Zhong said. "Our cells are staying within the ectoderm lineage."Zhong said he expects that suppressing other oncogenes in other families of cells would have the same effect, which could have critical significance for stem cell therapy. Future research should focus on determining which genes to manipulate, Zhong said.The study is slated to appear in the Proceedings of the National Academy of Sciences later this month, according to AAAS.

SAN FRANCISCO, Aug. 22 (Xinhua) -- Hewlett-Packard (HP) on Monday unveiled a new business desktop computer, days after the world's largest personal computer (PC) maker announced its plan to sell its PC business.The company said the new model, HP Compaq 8200 Elite All-in-One Business Desktop, is the industry's first all-in-one PC that integrates Intel's second-generation Core vPro technology, which can deliver up to 40 percent better performance, 15 percent faster hard drive access and reduced downtime via remote information technology management."Another industry first in our Elite desktop family demonstrates our commitment to engineering excellence and underscores our global leadership in secure, enterprise computing, " Jeff Groudan, HP's director of commercial desktop marketing, said in a statement.HP said the new computer is available now in the United States. It starts at the price of 999 U.S. dollars, and comes with a standard three-year warranty.Last Thursday the company announced that it is considering a full or partial separation of its PC business through a spin-off or other transactions, a process that HP estimates may take about 12 to 18 months.
WASHINGTON, June 15 (Xinhua) -- Using the deepest X-ray image ever taken, astronomers found the first direct evidence that massive black holes were common in the early universe, the U.S. National Aeronautics and Space Administration (NASA) said Wednesday in a statement.The discovery from NASA's Chandra X-ray Observatory shows that very young black holes grew more aggressively than previously thought, in tandem with the growth of their host galaxies.By pointing Chandra at a patch of sky for more than six weeks, astronomers obtained what is known as the Chandra Deep Field South (CDFS). When combined with very deep optical and infrared images from NASA's Hubble Space Telescope, the new Chandra data allowed astronomers to search for black holes in 200 distant galaxies, from when the universe was between about 800 million to 950 million years old."Until now, we had no idea what the black holes in these early galaxies were doing, or if they even existed," said Ezequiel Treister of the University of Hawaii, lead author of the study to appear Thursday in journal Nature. "Now we know they are there, and they are growing like gangbusters."The super-sized growth means that the black holes in the CDFS are less extreme versions of quasars -- very luminous, rare objects powered by material falling onto supermassive black holes. However, the sources in the CDFS are about a hundred times fainter and the black holes are about a thousand times less massive than the ones in quasars.The observations found that between 30 and 100 percent of the distant galaxies contain growing supermassive black holes. Extrapolating these results from the small observed field to the full sky, there are at least 30 million supermassive black holes in the early universe. This is a factor of 10,000 larger than the estimated number of quasars in the early universe."It appears we've found a whole new population of baby black holes," said co-author Kevin Schawinski of Yale University. "We think these babies will grow by a factor of about a hundred or a thousand, eventually becoming like the giant black holes we see today almost 13 billion years later."
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