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SINGAPORE, Sept. 7 (Xinhua) -- Singapore scientists have found possible new ways to treat a type of aggressive breast cancer that is unresponsive to current forms of treatment, local broadcaster Channel NewsAsia reported on Wednesday.The team of scientists at the Genome Institute of Singapore ( GIS) and National University of Singapore (NUS), led by GIS senior group leader Qiang Yu, found that the enzyme EZH2 acts by inhibiting genes that stop the growth of tumors in the body.The insights could open the door to developing more effective treatment for fast spreading breast cancers, especially the estrogen receptor-negative breast cancer that is common all over the world.It was also found that through EZH2, cancer is promoted in the body by activating specific genes that impact breast cancer progression and cancer stem cell self-renewal.Yu said the new understanding on how EZH2 works as a cancer- causing gene in breast cancer has important therapeutic implication."The results suggest that small molecule drugs that block enzyme activity of EZH2 may not work for cancers caused by EZH2's activation genes," Yu said.Currently pharmaceutical companies have been developing drugs only to the block EZH2 enzyme activity so that tumor suppressers can perform their protective role in blocking cancer growth.Researchers said the next step would be to develop biomarkers to identify tumors with EZH2.This step would enable better treatment methods, with one of options being the development of therapies that shut down EZH2 completely and not just inhibit its enzymatic function.The findings have been published on the journal Molecular Cell.

WASHINGTON, Sept. 14 (Xinhua) -- Controlling diabetes may someday involve mining stem cells from the lining of the uterus, Yale School of Medicine researchers report in a new study published Wednesday in the journal Molecular Therapy. The team treated diabetes in mice by converting cells from the uterine lining into insulin-producing cells.The endometrium or uterine lining, is a source of adult stem cells. These cells generate uterine tissue each month as part of the menstrual cycle. Like other stem cells, however, they can divide to form other kinds of cells.Led by Yale Professor Hugh Taylor, the researchers bathed endometrial stem cells in cultures containing special nutrients and growth factors. Responding to these substances, the endometrial stem cells adopted the characteristics of beta cells in the pancreas that produce insulin. Over the course of a three- week incubation process, the endometrial stem cells took on the shape of beta cells and began to make proteins typically made by beta cells. Some of these cells also produced insulin.After a meal, the body breaks food down into components like the sugar glucose, which then circulates in the blood. In response, beta cells release insulin, which allows the body's cells to take in the circulating glucose. In this study, Taylor and his team exposed the mature stem cells to glucose and found that, like typical beta cells, the cultured cells responded by producing insulin. The team then injected diabetic mice with the mature, insulin-making stem cells. The mice had few working beta cells and very high levels of blood glucose.Mice that did not receive the stem cell therapy continued having high blood sugar levels, developed cataracts and were lethargic. In contrast, mice that received the cell therapy were active and did not develop cataracts, but the animals' blood sugar levels remained higher than normal.The Yale team's findings suggest that endometrial stem cells could be used to develop insulin-producing islet cells, which are found in the pancreas. These islet cells could then be used to advance the study of islet cell transplantation to treat people with diabetes.Taylor said in a statement that the next step in the research will be to verify how long this treatment remains effective.

WASHINGTON, June 16 (Xinhua) -- Cells in the human body are constantly being exposed to stress from environmental chemicals or errors in routine cellular processes. While stress can cause damage, it can also provide the stimulus for undoing the damage. New research by a team of scientists at the University of Rochester has unveiled an important new mechanism that allows cells to recognize when they are under stress and prime the DNA repair machinery to respond to the threat of damage.Their findings will be published Friday in journal Science. Cells in the human body are constantly being exposed to stress from environmental chemicals or errors in routine cellular processes. While stress can cause damage, it can also provide the stimulus for undoing the damage.The scientists, led by biologists Vera Gorbunova and Andrei Seluanov, focused on the most dangerous type of DNA damage -- double strand breaks. Unrepaired, this type of damage can lead to premature aging and cancer. They studied how oxidative stress affects efficiency of DNA repair. Oxidative stress occurs when the body is unable to neutralize the highly-reactive molecules, which are typically produced during routine cellular activities.The research team found that human cells undergoing oxidative stress synthesized more of a protein called SIRT6. By increasing SIRT6 levels, cells were able to stimulate their ability to repair double strand breaks. When the cells were treated with a drug that inactivated SIRT6, DNA repair came to a halt, thus confirming the role of SIRT6 in DNA repair. Gorbunova notes that the SIRT6 protein is structurally related to another protein, SIR2, which has been shown to extend lifespan in multiple model organisms."SIRT6 also affects DNA repair when there is no oxidative stress," explains Gorbunova. "It's just that the effect is magnified when the cells are challenged with even small amounts of oxidative stress."SIRT6 allows the cells to be economical with their resources, priming the repair enzymes only when there is damage that needs to be repaired. Thus SIRT6 may be a master regulator that coordinates stress and DNA repair activities, according to Gorbunova.

coastline in the U.S. State of California sampled by the state water board harbored fish with mercury in such high concentrations that they shouldn't be eaten by young women and children, a newly released survey has found.Fourteen percent of locations had similarly elevated levels of PCBs, according to the survey published by The Los Angeles Times on Sunday.The most elevated concentrations of mercury and PCBs were found in San Francisco Bay and San Diego Bay, said the survey funded by the state water board.The findings, part of a two-year inquiry that is the largest statewide survey of contaminants in sport fish along the California coast, examined more than 2,000 fish from three dozen species gathered in 2009 from waters near Los Angeles, San Francisco and San Diego, the paper said.The survey highlights the health problem of lingering mercury, a poisonous metal that is found in fish globally, and of PCBs, toxic chemicals the United States banned in the 1970s, the report said.Both substances continue to pose a risk to people who eat fish caught along the California coast because they can lead to nervous system damage and developmental problems in children and can cause cancer, liver damage and reproductive harm, the report quoted researchers as saying."Unfortunately, we're not seeing many areas that are totally clean," said Jay Davis, a senior scientist for the San Francisco Estuary Institute and lead author of the study. But a catalog of where and in what fish the substances abound should help anglers make better choices, Davis said. "With good information, people can reduce their exposure significantly."Sharks had some of the highest levels of mercury because of their unusual tendency to accumulate contaminants in their flesh, while chub mackerel had the lowest levels of contamination, according to the survey.The survey results were used in part to help craft new fish consumption guidelines issued earlier this week for anglers in San Francisco Bay, the first update there by state health officials in 17 years. The advisory identifies shiner perch and other surf perches as unsafe to eat in any quantity and warns young women and children not to eat white sturgeon, striped bass and sharks caught in the bay, The Times said.The buildup of metals and other chemicals in fish is such a problem along the Southern California coast that health officials two years ago expanded the number of fish species on the "do not eat" list from one to five because of high levels of PCBs, mercury and the banned pesticide DDT, the report noted.

WASHINGTON, Sept. 12 (Xinhua) -- An enzyme that appears to play a role in controlling the brain's response to nicotine and alcohol in mice might be a promising target for a drug that simultaneously would treat nicotine addiction and alcohol abuse in people, U.S. researchers find.Over the course of four weeks, mice genetically engineered to lack the gene for protein kinase C (PKC) epsilon consumed less of a nicotine-containing water solution than normal mice, and were less likely to return to a chamber in which they had been given nicotine. In contrast, normal mice steadily increased their consumption of nicotine solution while the mice lacking PKC epsilon did not.The study conducted by researchers at the Ernest Gallo Clinic and Research Center, affiliated with the University of California, San Francisco, appeared Monday in the online edition of the Proceedings of the National Academy of Sciences.In normal mice, as in humans, nicotine binds to a certain class of nicotinic receptors located on dopamine neurons, which causes dopamine to be released in the brain. Dopamine creates a feeling of enjoyment, and thus prompts a sense of reward. Researchers found that mice lacking PKC epsilon are deficient in these nicotinic receptors.The finding complements earlier research in which researchers found that mice genetically engineered to lack the PKC epsilon enzyme drank less alcohol than normal mice and were disinclined to return to a chamber in which they had been given alcohol."This could mean that these mice might not get the same sense of reward from nicotine or alcohol," said Gallo senior associate director and investigator Robert Messing. "The enzyme looks like it regulates the part of the reward system that involves these nicotinic receptors."The reward system is a complex of areas in the brain that affect craving for nicotine, alcohol and other addictive substances.The next step in the research, said Messing, would be to develop compounds that inhibit PKC epsilon. The ultimate goal, he added, would be medications that could be used "to take the edge off of addiction by helping people get over some of their reward craving."

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