Canadian scientists discover "youth gene"
TORONTO -- June 2, 1998
We look at death as - well - a fact of life. But while the mechanics of dying have been documented, answers to the "why" of expiry have remained elusive. Now a Canadian research team has found there's a genetic component to the mortality puzzle. In other words, death is somewhat hereditary. Aging is caused when body cells like these bone cells are damaged by the oxygen that, ironically, they need to survive The team, led by Dr. Gabrielle Boulianne of the Hospital for Sick Children and the University of Toronto, and Dr. John Phillips of the University of Guelph began their research to look at why oxygen -- the compound cells use to extract energy from food -- is toxic. "It's an irony that while our cells require oxygen, it's toxic to those same cells," Dr Phillips says. "In order to survive, we must detoxify the oxygen before using it, and our detox mechanism is not perfect." The scientists set up experiments to examine why organisms with long life spans, such as humans, use oxygen more efficiently than those with short life spans, such as fruit flies. As a result of those experiments, the researchers were able to identify a gene, called SOD1, that produces the enzyme superoxide dismutase, an oxygen detoxifier. Could introduction of a new gene into motor neurons, pictured above, be the key to immortality? But the really astounding discovery came when the scientists introduced the gene into fruit flies' motor neurons, cells which connect an organism's brain to the nerves controlling its muscles. "Motor neurons, the cells which are damaged in spinal injuries or lost in Lou Gherig's disease, do not normally have the SOD1 gene," says Dr. Phillips. "But when we introduced it into the flies' motor neurons, their life span increased 40 percent." Not only did the fruit flies live longer - they really lived. "Fruit flies have the same pattern of aging as humans, losing muscle strength, interest in sex and the ability to reproduce as they grow older," Phillips notes. "When SOD1 was introduced into their motor neurons, the fruit flies did not just have an extended old age, they had a postponement of senescence - an extended youthfulness." The discovery of the SOD1 effect on motor neurons means a whole different way of looking at aging, according to Dr. Boulianne. "We now know that just one gene, targeting one type of cell has a huge impact on aging," says Dr. Boulianne. "Contrary to what was previously thought, that many factors contribute to aging, it now appears that the process may be simpler." Dr. Phillips says SOD1's action of postponing cell degeneration means the discovery has "very promising" applications to research into human aging. "We are now on the search for other cell types which will respond to the gene, and for other genes which may produce similar results," Dr. Phillips says. "We also want to see if it works in vertebrate mammals such as mice." The study is published in the June issue of the scientific journal Nature
Cancer find could spell early detection
LOS ANGELES -- Jan. 7, 1998
The finding of a possible trigger of one of the earliest detectable signs of cancer could lead to better ways to detect and treat the often deadly disease. In a report to be published in the Journal of Molecular Biology, researchers from the City of Hope Cancer Center in Los Angeles say they have new evidence that abnormal DNA structures may be responsible for a chemical change that appears to be a precursor to cancer development. The deviant structures, called hairpins or loops, can result from errors committed during the replication of the master double-helix molecule that contains the genetic blueprint and controls the activity of a cell. Steven Smith, director of the Department of Cell and Tumor Biology, says, ''The DNA molecule normally has the same double-helical shape regardless of the genetic information it encodes. The abnormal structures we have been studying are like knots, hairpins or loops _ parts of the DNA molecule actually fold back on themselves.'' These structures have been shown in past studies to occur in oncogenes and other cancer genes as well as in genes implicated in other diseases, such as Fragile X syndrome, an inherited form of mental retardation, and Huntington's chorea, a neurological disorder. Under normal circumstances, the abnormalities are removed by the cell's repair mechanisms. But when these fail, the structures remain, eventually contributing to mutation and cancer development. Smith says, ''We've found these abnormal DNA structures can account for one of the earliest detectable chemical changes in malignant cells _ alterations in the pattern by which small chemical groups are attached to the DNA molecule.'' Smith tells UPI, ''Once you understand the concept, you can use this understanding to develop better testing techniques and, ultimately, to improve prognosis, outcomes and treatment options.'' He says in an interview the abnormalities were noted in every cancer studied, including breast, colon, lung and prostate. Smith says the work could lead to the development of methods for diagnosing cancer at its earliest stage - when it's easiest to treat.
Anti-Cancer Medicines, Research
Progressing
BEIJING -- Sept. 2, 1997
Chinese pharmaceutical manufacturers will put more time, talent and money into researching world-level, anti-cancer traditional Chinese medicines, according to today's "China Daily". The State Administration of Traditional Chinese Medicine (SATCM) is scheduled to develop several such medicines before the turn of the century -- used to help alleviate cancer victims' pain around the world, said Yu Shenglong, SATCM deputy director. The World Health Organization (WHO) statistics indicate more than six million people died from various forms of cancer in the world last year. In China, 1.6 million cancer cases are reported annually. Cancer is the second leading cause of death in the country, behind heart and brain vascular diseases. More than two million patients currently suffer from malignant tumors. One in 200 Chinese families is affected. However, only 20 percent receive surgery, due to various reasons, including financial and physical situations. Between 10 and 15 percent are suitable for chemical and radiation therapies, known to cause side effects, said Hong Jing, SATCM official in charge of scientific research. China began researching anti-cancer medicines from Chinese herbs in the 1950s, Hong said. Some 3,000 herb varieties were tested. Of those, 200 were deemed effective in improving patients' physical conditions. Nearly 100 of the drugs have been approved and are being used clinically. Scientists have so far developed 20 preparations out of Chinese herbs. Five have been recognized as new traditional Chinese medicines by the State. Autoimmunity Gene DiscoveredScientists have discovered the first example of a gene solely responsible for an autoimmune disease, a type of disorder in which the immune system attacks the body. The finding, announced 31 October at the annual meeting of the American Society for Human Genetics in Baltimore, Maryland, is expected to lead to a better understanding of many forms of autoimmunity, including common ones such as multiple sclerosis and rheumatoid arthritis, whose causes are largely mysterious. The findings pinpoint the gene behind a rare disease with a jawbreaking name: autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED). In the malady, a victim's immune system attacks hormone-producing organs such as the pancreas and the thyroid, parathyroid, and adrenal glands, often rendering them nonfunctional. People with APECED also often suffer from chronic fungal infections in their mouths and other mucous membranes, and hair loss. Unlike other autoimmune disorders with associated risk factors, APECED is clearly caused by a mutation in a single gene, based on analyses of affected families. The search for the gene began in Finland, whose isolated population has often been studied for its elevated rate of rare genetic diseases. Leena Peltonen, of the National Public Health Institute in Helsinki, and her colleagues, studied 14 Finnish families with 23 members afflicted with APECED. By 1994, Peltonen's group had homed in on a region on chromosome 21 that likely contained the mutated gene. After that publication, Peltonen teamed up with Marie-Laure Yaspo and her group at the Max Planck Institute for Molecular Genetics; and a second international collaboration, led by Nabuyoshi Shimizu in Japan, Stylianos Antonarakis in Switzerland, and Kai Krohn in Finland, began hunting for the gene. The race was on, with the two teams probing for candidate genes in that region to determine which bore the APECED mutations. Now the race has ended in a tie. Both groups announced they have found the gene and will soon publish their results. They don't know the purpose of the protein it encodes. However, in the presentations, speakers for both teams said that two stretches of the gene code for so-called zinc fingers--protein structures that insert themselves into the grooves of DNA--suggesting that the encoded protein probably turns other genes on and off. The teams disagree, however, about where the gene is expressed. Peltonen's group found that the gene is turned on in "a wide variety of tissues," while Shimizu's group found it active significantly only in the thymus, lymph nodes, and fetal kidney cells--all areas important for the development of the immune system's T cells. The find is a welcome booster shot for autoimmune research. "We don't have very many insights into autoimmune disease," says Victor McKusick, of Johns Hopkins University, who is compiling a massive database of inherited characteristics.
*MUCH MORE TO COME
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