Articles tagged with Dna Damage
Researchers found that blood stem cells, which are among the smallest cells in the body, lose their ability to perform their normal function — replenishing the body’s blood cells — as they grow larger. However, when the cells were restored to their usual size, they behaved normally again.
Researchers have developed a simple, postal urine test that can detect signs of urothelial cancer in Lynch Syndrome (LS) patients, who are at high risk of developing tumors. The test uses cell-free DNA shed into the urine to identify DNA from tumor cells with characteristic microsatellite instability.
Researchers at Johns Hopkins Kimmel Cancer Center found a new treatment option for inoperable pleural mesothelioma using immunotherapy agent durvalumab combined with platinum-based chemotherapy. Patients with epithelioid tumors experienced higher survival rates, including some who remained tumor-free after completing the trial.
GIST scientists utilized latest advances in single molecule detection to observe the enzymatic activity of gene repair. The study revealed that ExoIII has an affinity for damaged DNA sites, creating a gap that Pol I fills. Understanding this mechanism may lead to technologies for targeted gene repair and drug development.
Researchers found that UVB phototherapy increases levels of romantic passion and aggression in both men and women. Exposure to sunlight affects the endocrine system's regulation of sexual hormones.
Researchers identified DSS1 as a critical protein in breast cancer progression and found that depleting it makes cancer cells more responsive to lower doses of anti-cancer drugs. This technique may reduce drug-induced side effects in breast cancer patients, providing a safer treatment option.
Fels and Fox Chase researchers found specific TET2 and DNMT3A mutations in leukemia patients that affect DNA repair pathways. These mutations make leukemia cells sensitive to PARP inhibitors, a type of targeted therapy, while others are resistant. The study aims to develop personalized therapies for patients with these mutations.
Researchers found that UVB radiation from the sun causes chemical changes to DNA, leading to disease-causing mutations. This discovery sheds light on the origins of melanoma and highlights the importance of prevention efforts.
Research suggests that telomere shortening drives intestinal inflammation in inflammatory bowel disease (IBD). Telomere erosion is positively associated with disease severity and may underlie disease recurrence.
Researchers have developed a novel method for studying DNA repair in yeast cells that can be conducted entirely in space, using CRISPR/Cas9 genome editing technology. The technique successfully demonstrated the viability of the new method on the ISS, paving the way for extensive research into DNA repair in space.
A study from West Virginia University suggests that pollutant exposure can lead to increased free-radical damage, which speeds up aging. This occurs when pollutants break down into highly reactive molecules that damage biomolecules, leading to premature aging.
Researchers at Goethe University Frankfurt discovered that Nox4, an enzyme producing H2O2, prevents cancer by keeping phosphatases out of the cell nucleus, thus allowing DNA damage to be recognized and repaired. In its absence, mutated cells multiply uncontrollably, leading to tumour formation.
Scientists have identified specific regions within the DNA of neurons that accumulate a certain type of damage, which appears to be unique to neurons. This discovery challenges current knowledge about the cause of DNA damage and its potential implications in neurodegenerative diseases.
Researchers at Baylor College of Medicine have identified 25 rare genetic variants associated with increased risk of lung cancer. These variants, which include insertions and deletions, lead to genomic instability and increase DNA damage, suggesting a potential role in cancer development.
A research team from Cologne has discovered a mechanism that restores cell function after genome damage by altering the DNA structure. The discovery involves a double occupation of two methyl groups on the histone protein H3K4me2, which enables genes to be reactivated and proteins to be produced after damage.
New research reveals laundry lint can cause significant tissue damage in Mediterranean mussels, including deformity, swelling, and digestive tubule loss. The study also finds reduced filtering ability and increased DNA strand breaks.
A team of researchers at KIT demonstrated that DNA damage can occur up to 30 DNA building blocks away from the entry point of UV radiation. This finding has significant implications for understanding DNA photodamage and its role in skin cancer.
Studies published in the Journal of Experimental Medicine found that sticky webs of DNA released from immune cells cause much of the tissue damage associated with severe COVID-19. Blocking the release of these DNA webs could be a new therapeutic target for managing severe forms of the disease.
A team of scientists has discovered how the enzyme SPRTN recognizes and cleaves DNA-protein crosslinks, which are formed when proteins attach to DNA. This new mechanism is crucial for cell viability and the suppression of tumorigenesis, and has implications for cancer therapy.
Researchers discovered that DNA damage in moss Physcomitrella patens causes cells to reprogram into stem cells, producing an entire plant body. This phenomenon is a new adaptive strategy for plants under harsh environments.
Researchers have discovered how XPG binds to and reshapes damaged DNA, illuminating its role in maintaining genetic stability. The protein's unique 'sculpting' activity allows it to bend DNA, recruiting proteins to fix damage, and may help prevent cancer by supporting homologous recombination.
Researchers found persistent DNA damage in placentas of mice with cohesin mutations, leading to senescence and pro-inflammatory cytokines affecting embryonic growth. Targeting cytokine signaling may be a way to protect the health of the placenta and promote healthy pregnancies.
Researchers screened 163,000 DNA mutations in C. elegans roundworms to understand the interplay between DNA damage and faulty repair systems. The study found that multiple DNA repair pathways work together to prevent mutagenesis, and a single mutagen can leave varying mutational signatures depending on the faulty repair system.
A research group at Kumamoto University has discovered a novel gene, C19ORF57, involved in meiotic recombination during sperm production. The gene plays a crucial role in repairing DNA damage, which is essential for maintaining male fertility.
A Monash University study found that inhibiting cell death pathways in oocytes allows them to rapidly repair DNA damage, maintaining fertility. Double-strand breaks are the most harmful type of DNA damage, promoting genetic instability if not repaired correctly.
Researchers discovered that aging neurons accumulate DNA damage, particularly oxidative 8-oxo-guanine lesions. Reactivating the enzyme HDAC1 can help repair this damage and improve cognitive function in mice.
Researchers at the University of Virginia Health System have made a groundbreaking discovery suggesting that improper cellular cleanup during brain development may cause lifelong behavioral issues. This process, mediated by the AIM2 inflammasome, plays a critical role in ensuring proper brain assembly and function.
A study found that low-dose chest CT scans used for lung cancer screening do not cause significant DNA damage or chromosome aberrations. The results suggest that the risks of low-dose CT are minimal, and it can be used for lung cancer screening.
Researchers have discovered two mechanisms that repair DNA damage caused by acetaldehyde, a degradation product of alcohol. The novel route cuts the crosslink itself, providing a new line of defense against alcohol-induced ICLs.
Researchers found unique DNA damage patterns in cells lining the gut and bowel cancer tumours, linked to a specific strain of E. coli toxin colibactin. The discovery could enable early detection and prevention of bowel cancer through targeted screening tests.
The study demonstrates that MLN4924 treatment induces DNA damage and accumulates cells in S phase, enhancing sensitivity when combined with cisplatin. In vivo results show reduced tumor growth in a NOD-SCID mouse xenograft model treated with MLN4924 alone or in combination with cisplatin.
Researchers at the University of Toronto have found a complex system of filaments and liquid droplet dynamics that enables the repair of damaged DNA in cell nuclei. This discovery challenges previous assumptions about DNA damage and highlights the value of cross-disciplinary research.
Researchers extracted DNA from museum specimens using a vortex fluidic device (VFD), accelerating the process from days to hours. The breakthrough enables exploration of historical and extinct species' genetic information, shedding light on human impact on ecosystems.
A new screening method developed by MIT biological engineers can detect DNA damage in cells, which can predict cancer development. The test uses human liver-like cells and has enhanced sensitivity, detecting all nine chemicals tested.
New study from the Francis Crick Institute reveals that telomere t-loops are crucial for protecting chromosomes from damage by adopting a lasso-like structure. The research also uncovered the mechanism that regulates the winding and unwinding of these t-loops, essential for maintaining chromosome integrity.
Scientists from the University of Copenhagen have identified two proteins, 53BP1 and RIF1, that orchestrate the repair of damaged DNA by building a three-dimensional scaffold around broken strands. This scaffold concentrates special repair proteins, enabling cells to prevent collateral damage and maintain genetic stability.
Researchers have discovered how certain proteins orchestrate repair of damaged DNA by building a three-dimensional scaffold that concentrates special repair proteins. This discovery has significant implications for understanding how DNA damage causes disease and designing treatments for patients with unstable DNA.
Researchers have identified colibactin-645 as the culprit of DNA double-strand breaks, revealing a new link between E. coli toxins and colorectal cancer risk. The discovery provides a model for designing potent DNA cleaving agents.
A new method has been developed to improve the quality of stem cell-derived cardiomyocytes, which can be used to treat heart attacks. The approach, tested in a mouse heart attack model, doubled the engraftment rate of injected cells, showing promise for repairing damaged heart tissue.
A protein called UV-DDB has been found to identify and supervise the repair of DNA damage, suggesting a key role in maintaining genome stability. The discovery sheds light on why some individuals with a rare genetic disorder are more susceptible to cancer.
A new study found that Slug promotes breast stem cell health by repairing DNA damage, and its deficiency is linked to increased DNA damage and decreased stem cell activity in both young and aged breast tissue. This suggests that Slug functions as a safeguard against age-related decline of breast stem cell function.
A Baylor University researcher has made a significant discovery about the dynamic process of DNA damage recognition, providing new insights into the molecular repair machinery. The study found that the protein Rad4/XPC binds to UV-induced DNA lesions, marking them for repair and initiating the nucleotide excision repair pathway.
A study found that telomere shortening rate predicts species lifespan, rather than initial telomere length. Body weight and heart rate were less powerful predictors of lifespan.
Researchers discovered that bats have higher levels of ABCB1 protein, which reduces DNA damage and cancer incidence. Blocking ABCB1 in bat cells triggers toxic chemical accumulation, leading to cell death. This finding could lead to future therapies for humans to prevent or treat cancer.
DNA damaged by cisplatin is mostly fixed within two circadian cycles in noncancerous tissue, with repair of transcribed genes dominating the first 48 hours. This knowledge could aid the design of successful chronochemotherapies to reduce toxicity and target cancer cells.
Researchers from the Thomä group at FMI have identified a new mechanism by which UV-DDB detects and binds to damaged DNA tightly packed in nucleosomes. This mechanism, known as 'slide-assisted site-exposure', allows repair proteins to bind to lesions without requiring additional proteins or chemical energy.
A protein complex, Ccr4-Not, has been shown to recruit factors that mark RNAPII with ubiquitin, triggering its degradation and clearing the jam. This process is essential for normal cell function and preventing diseases associated with DNA damage.
Researchers found that combining adavosertib with irinotecan, navitoclax or capecitabine increased its effectiveness against pancreatic cancer. The study aimed to identify new combinations of drugs to enhance adavosertib's effect.
Research suggests that sperm DNA damage in male partners may cause recurrent pregnancy loss (RPL), with affected men having twice as much DNA damage as healthy counterparts. High levels of reactive oxygen species were also found, which can damage cells like sperm.
Researchers have discovered that sperm DNA taken directly from the testicles of infertile men is as good as that of ejaculated sperm from fertile men, potentially opening a new way for treatment. This finding may explain a major cause of male infertility and could lead to improved fertility outcomes.
Researchers at Bar-Ilan University identified a beneficial role of sleep in clearing out DNA damage accumulated during waking hours. Sleep increases chromosome dynamics, which helps to repair and maintain the integrity of individual neurons.
A new study reveals a specific mechanism in human cells that delay propagation of DNA damage, giving cells a chance to stop piling up mutations. The discovery relies on precise timing and control inside the cells and identifies key molecular proteins involved in repairing DNA lesions.
A new study from the University of Copenhagen has identified a key mechanism behind the repair of human DNA damage, which can lead to cancer. The researchers have discovered a protein called BARD1 that acts like a 'scanner' to launch the flawless DNA repair system.
Researchers discovered a link between Escherichia coli and colorectal cancer risk through colibactin, a genotoxic warhead that damages DNA. The study identified potential biomarkers for assessing colorectal cancer risk and provides significant mechanistic insights into the carcinogenic activities of colibactin.
Researchers studied how colibactin damages DNA and created a novel technique to identify DNA adducts. They isolated and characterized the products of the reaction with DNA, revealing a cyclopropane ring structure that forms the colibactin warhead.
A new study found that sleep deprivation can cause DNA damage in healthy individuals, increasing the risk for cancer, cardiovascular, metabolic, and neurodegenerative diseases. Even a single night of sleep deprivation can trigger events contributing to chronic disease development.
A team of researchers used bacteria to identify human proteins that cause DNA damage when overproduced, leading to cancer. The study found 284 human protein relatives linked to cancer more often than random sets of proteins.
Scientists discovered that DNA damage, not just errors in DNA doubling, causes many genetic mutations. This challenge traditional views on mutagenesis and its role in hereditary diseases and cancer.
David A. Sinclair and Laura Niedernhofer received the Irving S. Wright Award of Distinction and Vincent Cristofalo Rising Star Award in Aging Research, respectively, for their groundbreaking work on age-related processes and DNA damage. The awards recognize their contributions to advancing the field of aging research.
Houston Methodist researchers have identified a repair defect in nerve cells that sends messages to the brain, potentially leading to a therapy for preventing or slowing down ALS. The team discovered a DNA Ligase-targeted therapy could inhibit oxidative damage repair in Amyotrophic Lateral Sclerosis.