Articles tagged with Telomerase
Researchers have solved the structure of an essential RNA domain in telomerase, a crucial enzyme in cancer cell division. The discovery provides insights into how telomerase works and could lead to targeted drug interventions.
Scientists isolated immune cells from HIV-infected persons and cultured them with chemical compounds, producing the same changes as gene therapy. The findings offer a new approach to strengthen the immune system's capacity to stave off HIV.
Chronic stress, even in healthy women, can lead to shorter telomeres and increased oxidative stress, accelerating cellular aging. The study also found that caregivers of chronically ill children experienced more stress and shorter telomeres than controls.
Researchers have discovered the structure of human POT1, a protein that caps the ends of chromosomes and regulates telomere length. The protein binds to a ten-nucleotide sequence, protecting the telomere from erosion, and its structure suggests that telomerase activity is regulated by this complex.
Researchers at UCLA have discovered a protein that can keep HIV-fighting cells youthful and active, dividing endlessly and preventing telomeres from shortening. This breakthrough could lead to the development of new treatments for AIDS, cancer, and other diseases.
A retrospective study from St. Jude Children's Research Hospital found that high levels of telomerase gene expression are associated with an unfavorable outcome for children treated for osteosarcoma, including lower progression-free survival rates and decreased overall survival.
Recent findings by scientists at Lawrence Berkeley National Laboratory and University of California, San Francisco, reveal telomere crisis as a key event in breast cancer progression. The researchers found that telomere length decreases in hyperplasia, carcinoma in situ, and invasive cancers, indicating increased genomic instability.
Researchers at UT Southwestern Medical Center have discovered that certain enzyme inhibitors can slow tumor growth by inhibiting telomerase, an enzyme that maintains DNA sequences. The study found that these inhibitors can be used in combination with standard cancer therapies to slow or prevent recurrence of tumors.
Researchers used RNA interference to impair cancer cells' ability to produce telomerase, resulting in a 85% shortening of telomeres over 75 days. The technique reduces but doesn't fully block telomerase production, paving the way for potential therapy against most cancers.
Cancer cells have evolved to continually activate telomerase, keeping telomeres intact and enabling rapid division. Researchers at UC Berkeley are now searching for proteins and signals involved in telomerase shuttling around the cell nucleus to develop new therapeutic strategies.
Researchers at Princeton University discovered a new activator protein Est1 that plays a key role in telomere capping. This finding contradicts existing theories and may offer a new target for cancer treatment. Est1 works by sweeping in with precise timing to activate the telomere-building process.
Researchers at the University of Illinois have developed a simple protein test to detect telomerase activity in cancerous cells of dogs and cats. The test has shown promising results in diagnosing malignant tumors in pets, with high accuracy rates compared to traditional diagnostic methods.
Telomeres, protective caps on chromosome ends, are shorter in people exposed to arsenic, increasing cancer risk. Long-term arsenic exposure has been associated with accelerated telomere shortening, a potential biomarker for arsenic poisoning.
The study found that critically short telomeres signal cells to arrest or die, rather than average length. Turning on telomerase can restore function without significantly increasing overall telomere length, offering new insights into cancer treatment options.
Researchers discovered that introducing a tiny mutation in the telomerase enzyme can trigger a DNA damage response, inducing cell-cycle arrest or cell death in human cancer cells. This approach could lead to a new therapeutic strategy for cancer treatment.
A Princeton scientist has discovered a naturally occurring protein that inhibits telomerase, which replicates and lengthens chromosome ends. The protein, Pif1p, acts directly on the chromosome ends to keep the lengthening process in check.
Researchers found that telomerase expression can activate the c-myc oncogene, a hallmark of cancer cells. This raises concerns about using telomerase in human tissue culture cells for therapeutic purposes.
Researchers found that telomerase blocks a biochemical cascade of reactions called apoptosis, which causes nerve cell self-destruction. High levels of telomerase display remarkable resistance to damage or death in experimental models of Alzheimer's disease or stroke.
A new prototype vaccine activates cytotoxic T-lymphocytes to destroy cancer cells using telomerase as a target. The vaccine has shown promise in both human and transgenic mice, indicating potential effectiveness against various types of cancer.
Researchers at Johns Hopkins describe fundamental shape of telomerase molecule in mammals and other vertebrates, identifying four common areas highly involved with the enzyme's working. This new information may prompt approaches to inhibit the enzyme, which is active in cancer cells and contributes to their continuous cell division.
Researchers at UT Southwestern Medical Center designed and tested synthetic inhibitors against telomerase, a key enzyme in cancer cell immortality. These inhibitors successfully caused progressive telomere shortening and cell death in human breast and prostate cancer cells.
Researchers at Whitehead Institute successfully transformed normal human cells into cancer cells, shedding light on the complex process of tumor development. The new cell lines offer a unique window into the biochemical and physiologic changes that occur during cancer formation.
Scientists find that telomerase enzyme contributes to chromosome stability beyond telomere length, offering a new target for extending cell life span and combating cancer. The discovery suggests a novel approach to manipulating the enzyme for therapeutic purposes.
Mice lacking a gene for making telomeres displayed symptoms of aging, including graying hair and increased tumor incidence. However, the study reveals that telomere loss is not solely responsible for aging, suggesting other mechanisms at play.
Researchers demonstrate that human cells grown in the laboratory and immortalized by telomerase are not transformed into cancer cells, exhibiting normal behavior despite extended lifespan. The findings hold promise for new therapies for age-related diseases and cancer.
This book brings together international specialists to discuss the genetic structure of telomeres, telomerase function, and their importance in aging and cancer. The chapters cover topics such as telomere length regulation, chromosome end replication, and telomerase repressor genes.
Researchers at UT Southwestern Medical Center discover that telomerase causes human cells to retain their youth and continue dividing beyond their normal limit. The extension of normal cell lifespan in a youthful state presents numerous opportunities for biotechnology and medicine, including producing engineered products in human cells.
Researchers have identified a crucial telomerase subunit, hEST2, expressed in primary human tumors but undetectable in normal tissues. This discovery paves the way for developing anti-telomerase drugs to target cancer cells and halt their immortal growth.
A research team has discovered a key gene in the human telomerase enzyme, which could aid in diagnosing cancer. The discovery also provides opportunities for developing new treatments by inhibiting the enzyme.
Researchers have identified a key protein in the telomerase enzyme that is selectively activated in many cancer cells. The discovery may lead to the development of new anti-cancer agents, including variants of existing pharmaceuticals.