 |
|
Short chromosomes put cancer cells in forced rest
April 26, 2007A Johns Hopkins team has stopped in its tracks a form of blood cancer in mice by engineering and inactivating an enzyme, telomerase, thereby shortening the ends of chromosomes, called telomeres.
"Normally, when telomeres get critically short, the cell commits suicide as a means of protecting the body," says Carol Greider, Ph.D., the Daniel Nathans chair of molecular biology and genetics at Johns Hopkins. Her study, appearing online this month at Cancer Cell, uncovers an alternate response where cells simply - and permanently - stop growing, a process known as senescence.
In an unusual set of experiments, the research team first mated mice with nonoperating telomerase to mice carrying a mutation that predisposed them to Burkitt's lymphoma, a rare but aggressive cancer of white blood cells. Telomerase helps maintain the caps or ends of chromosomes called telomeres, which shrink each time a cell divides and eventually - when the chromosomes get too short - force the cell to essentially commit suicide. Such cell death is natural, and when it fails to happen, the result may be unbridled cell growth, or cancer.
The first generation pups born to these mice contained no telomerase and very long telomeres. These mice all developed lymphomas by the time they were 7 months old. The researchers then continued breeding the mice to see what would happen in later generations. By the fifth generation, the researchers discovered that the mice had short telomeres and stopped developing lymphomas.
When the researchers blocked the suicide machinery in these fifth-generation mice, they were very surprised to find that the mice still remained cancer free.
"We were confused as to what was going on; we thought for sure that blocking the cells' ability to commit suicide would lead to the cancer's returning," says Greider. A closer look showed microtumors in the mice's lymph nodes that had begun the road to cancer, but stopped, falling instead into a state of senescence.
"They don't die, they don't divide, they just sit there in permanent rest," says Greider. Greider, who won the Lasker Award in 2006 for her discovery of telomerase, says further study of the road to senescence should suggest new ways of preventing or treating cancer by interfering safely with telomerase and the cell-suicide system.
Johns Hopkins Medical Institutions
The first generation pups born to these mice contained no telomerase and very long telomeres. These mice all developed lymphomas by the time they were 7 months old. The researchers then continued breeding the mice to see what would happen in later generations. By the fifth generation, the researchers discovered that the mice had short telomeres and stopped developing lymphomas.
When the researchers blocked the suicide machinery in these fifth-generation mice, they were very surprised to find that the mice still remained cancer free.
"We were confused as to what was going on; we thought for sure that blocking the cells' ability to commit suicide would lead to the cancer's returning," says Greider. A closer look showed microtumors in the mice's lymph nodes that had begun the road to cancer, but stopped, falling instead into a state of senescence.
"They don't die, they don't divide, they just sit there in permanent rest," says Greider. Greider, who won the Lasker Award in 2006 for her discovery of telomerase, says further study of the road to senescence should suggest new ways of preventing or treating cancer by interfering safely with telomerase and the cell-suicide system.
Johns Hopkins Medical Institutions
Telomerase Current Events and Telomerase News RSSMice regain ability to extend telomeres suggesting potential for dyskeratosis congenita therapy
The human genetic disease dyskeratosis congenita (DKC) is an autosomal dominant disease that leads to abnormalities in tissues with a rapid cell turnover - the skin, nails, bone marrow, lungs and gut.
National Science Foundation congratulates Nobel Laureates in medicine/physiology, chemistry and economics
The National Science Foundation (NSF) congratulates the 2009 Nobel laureates, particularly those who have received NSF funding over the years: Jack W. Szostak, who shared the prize in physiology or medicine; Thomas A. Steitz, who shared the prize in chemistry; and Elinor Ostrom and Oliver E. Williamson who earned the Sveriges Riksbank Prize in economic sciences in memory of Alfred Nobel 2009.
Researchers examine mechanisms that help cancer cells proliferate
A process that limits the number of times a cell divides works much differently than had been thought, opening the door to potential new anticancer therapies, researchers at UT Southwestern Medical Center report in the Aug. 7 issue of the journal Cell.
Handle with care: Telomeres resemble DNA fragile sites
Telomeres, the repetitive sequences of DNA at the ends of linear chromosomes, have an important function: They protect vulnerable chromosome ends from molecular attack.
Variations in 5 genes raise risk for most common brain tumors
Common genetic variations spread across five genes raise a person's risk of developing the most frequent type of brain tumor, an international research team reports online in Nature Genetics.
Immune cells from patients with rheumatoid arthritis have prematurely aged chromosomes
Telomeres, structures that cap the ends of cells' chromosomes, grow shorter with each round of cell division unless a specialized enzyme replenishes them. Maintaining telomeres is thought to be important for healthy aging and cancer prevention.
Testes stem cell can change into other body tissues, Stanford/UCSF study shows
Scientists at the Stanford University School of Medicine and at UC-San Francisco have succeeded in isolating stem cells from human testes.
UT Southwestern researchers identify gene linked to inherited form of fatal lung disease
Researchers at UT Southwestern Medical Center have determined that a mutation in a gene known for its role in defending the lungs against invading pathogens is responsible for some inherited cases of a lethal lung disease affecting older adults. The same mutation may also be associated with lung cancer, the researchers said.
Researchers use chemical from medicinal plants to fight HIV
Like other kinds of cells, immune cells lose the ability to divide as they age because a part of their chromosomes known as a telomere becomes progressively shorter with cell division. As a result, the cell changes in many ways, and its disease fighting ability is compromised.
Scientists identify possible cause of endometriosis
Endometriosis is a condition whereby patches of the inner lining of the womb appear in parts of the body other than the womb cavity. It can cause severe pain and affects approximately 15% of women of reproductive age. Endometriosis is also associated with infertility, with 50% of infertile women affected by the condition.
More Telomerase Current Events and Telomerase News Articles
 |
Jan Marini Age Intervention REGENERATION BOOSTER for Science-Based Compound for Dramatically Younger Looking Skin by Jan Marini Skin Research Aging skin is still a reality, but the key to aging may reside in the ability to stabilize telomeres by allowing cells to "reset their aging clocks." Now our extraordinary new skin care compound captures the emerging science of topical Telomerase Enzyme as a realistic science-based option for dramatically younger looking skin. -Age Intervention Regeneration Booster combines Telomerase Enzyme in combination with anti-inflammatory agents, select peptides and other proven significant skin enhancing ingredients. An independent clinical study demonstrates measurable, significant and lasting improvements in the appearance of: Lines and wrinkles Elasticity Firmness Texture Discoloration Overall radiance, suppleness and hydration Each program consists of six mini-bottles, including one... |
 |
Telomeres and Telomerase in Aging, Disease, and Cancer: Molecular Mechanisms of Adult Stem Cell Ageing by K. Lenhard Rudolph (Author), K. Lenhard Rudolph (Editor) The understanding of the molecular mechanisms underlying the ageing process is essential to improve quality of life and health span in the growing populations of the elderly. Telomere shortening represents one of the basic aspects of ageing and telomere dysfunction could contribute to the accumulation of DNA damage during ageing. This book summarizes experimental evidence and clinical data indicating that telomere dysfunction influences human ageing, diseases and cancer. In addition, the book describes our current knowledge on checkpoints that limit cellular lifespan (senescence) and survival (apoptosis, crisis) in response to telomere dysfunction. A special focus of the book is on adult stem cells. There is emerging evidence that adult stem cell ageing impairs... |
 |
Telomeres and Telomerase: Methods and Protocols (Methods in Molecular Biology) by John A. Double (Author), Michael J. Thompson (Author) John A. Double and Michael J. Thompson have collected a critically important series of novel and essential techniques for studying telomeres and telomerase. These readily reproducible methods provide cutting-edge tools to identify, measure, and analyze telomeres, to determine telomerase expression at the RNA level, to determine telomerase activity, and to detect potential modifiers of this activity. The techniques for assaying telomerase activity range from standard radiological TRAP assays to nonradioactive methods, from non PCR-based methods to techniques using real-time PCR. Telomeres and Telomerase: Methods and Protocols provides the core array of productive techniques needed today to develop telomerase inhibitors or diagnostic/prognostic telomerase markers. |
 |
Telomeres and Telomerase - Symposium No. 211 by CIBA Foundation Symposium (Author) Telomeres and Telomerase Chairman: Sydney Brenner 1997 Telomeres are the protective genetic elements located at the ends of chromosomes and are essential for correct chromosomal structure and function. They are not fully replicated by the conventional DNA polymerase system because DNA synthesis occurs only in the 5??? to 3??? direction and requires an RNA primer for initiation. Consequently, cells require a special enzyme to maintain the telomeric ends of chromosomes during each round of replication. This enzyme, telomerase, is a ribonucleoprotein that extends chromosome ends by adding short stretches of nucleotide repeats using a portion of its integral RNA component as the template. Recently, much excitement has been generated by the suggestion that telomerase, or rather the absence of... |
 |
Telomeres and Telomerase in Cancer (Cancer Drug Discovery and Development) by Keiko Hiyama (Editor) Telomerase, an enzyme that maintains telomeres and endows eukaryotic cells with immortality, was first discovered in tetrahymena in 1985. In 1990s, it was proven that this enzyme also plays a key role in the infinite proliferation of human cancer cells. Now telomere and telomerase are widely accepted as important factors involved in cancer biology, and as promising diagnostic tools and therapeutic targets. Recently, role of telomerase in “cancer stem cells” has become another attractive story. Until now, there are several good books on telomere and telomerase focusing on biology in ciliates, yeasts, and mouse or basic sciences in human, providing basic scientists or students with updated knowledge. |
 |
Telomerase, Aging and Disease, Volume 8 (Advances in Cell Aging and Gerontology) by M.P. Mattson (Editor) This volume of Advances in Cell Aging and Gerontology critically reviews the rapidly advancing area of telomerase research with a focus at the molecular and cellular levels. The clearly established function of telomerase is to maintain chromosome ends during successive rounds of cell division by adding a six base DNA repeat on to the telomeric ends of chromosomes. As presented in the chapters of this volume, the mechanisms that regulate telomerase expression and activity are complex. Moreover, emerging data suggest additional roles for telomerase in the regulation of cell differentiation and survival.
|
 |
Telomeres and Telomerase: Reprint of Cytogenetic and Genome Research, Vol. 122, No. 3-4, 2008 by Predrag Slijepcevic (Editor) |
|
Extended life-spans. (includes related articles on longer lifespan and on telomerase discovery): An article from: The Futurist by Marvin Cetron (Author), Owen Davies (Author) This digital document is an article from The Futurist, published by World Future Society on April 1, 1998. The length of the article is 5684 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser. From the supplier: The discovery of melatonin as the hormone that has the ability to retard aging created an excitement in the scientific world as visions of humans living until the age of 120, 150, 200 or more can be made possible. Society, however, should prepare for the consequences of these breakthroughs. Citation Details Title: Extended life-spans. (includes related articles on longer lifespan and on... | |
 |
The Telomerase Project by William A. Gilmartin (Author) A secret project inside a cancer research company results in a remarkable discovery--a way to stop and reverse the aging process! But a power hungry venture capitalist and a government agency want to control it. The scientist behind the discovery is forced to disappear. His daughter and best friend become bait in a deadly manhunt that starts in Silicon Valley, moves into the high mountains of Colorado and ends in Washington D.C. Is the world ready for life ever lasting? Who gets to decide? |
![Telomerase-immortalized human fibroblasts retain UV-induced mutagenesis and p53-mediated DNA damage responses [An article from: DNA Repair]](http://ecx.images-amazon.com/images/I/51FZ3K9Y7XL._SL160_.jpg) |
Telomerase-immortalized human fibroblasts retain UV-induced mutagenesis and p53-mediated DNA damage responses [An article from: DNA Repair] by P.C. Porter (Author), D.R. Clark (Author), L.D. McDaniel (Author), McGregor (Author) This digital document is a journal article from DNA Repair, published by Elsevier in . The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser. Description: Immortalized cells frequently have disruptions of p53 activity and lack p53-dependent nucleotide excision repair (NER). We hypothesized that telomerase immortalization would not alter p53-mediated ultraviolet light (UV)-induced DNA damage responses. DNA repair proficient primary diploid human fibroblasts (GM00024) were immortalized by transduction with a telomerase expressing retrovirus. Empty retrovirus transduced cells senesced after a few doublings. Telomerase transduced GM00024 cells (tGM24) were cultured continuously for... |
| © 2009 BrightSurf.com |