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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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A recent study has identified a rare genetic mutation in three patients with early-onset acute myeloid leukaemia, highlighting the importance of DNA damage in driving cancer development. The study found that these patients lacked a DNA repair protein called MBD4, leading to increased DNA damage and accelerated ageing.
New research reveals that Rnf212 helps create a 'cellular memory' of DNA damage in oocytes, allowing cells to assess the severity of defects and prevent defective eggs from being formed. This process ensures that only high-quality eggs are selected for the ovarian reserve.
Scientists have discovered the unique characteristics of the Dps protein, which compacts bacterial DNA to protect it from damage. Despite compacting the DNA, the expression of genes remains unchanged. The study suggests that Dps may act as a shield to protect DNA while allowing bacteria to express genes necessary for survival.
Researchers found that e-cigarette users experience increased DNA damage related to acrolein exposure, which could increase their cancer risk. The study suggests that vaping may modify the genetic material in oral cells, highlighting the need for further research on the long-term health effects of e-cigarettes.
Researchers discovered an anti-cancer gene called LIF6 in elephants that helps destroy cells with damaged DNA, potentially preventing cancer. This gene emerged around 25-30 million years ago and may have played a key role in enabling the growth of modern elephants.
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Researchers at Mayo Clinic have discovered how the DNA repair protein 53BP1 relocates to chromosomes to fix damage, using RNA molecules as an off/on switch. This finding could lead to new therapies for ovarian cancer by targeting a specific protein called TIRR.
Researchers discovered that plant DNA repair works more efficiently on active genes, which are transcribed into RNA and proteins. The system's efficiency varies according to the day/night cycle, reflecting normal daily variations in transcription activity.
Chemotherapy-induced DNA damage triggers apoptosis in oocytes due to p63 activation. Researchers found that inhibiting specific enzymes can prevent this process, offering new hope for fertility preservation.
Research shows that nanoparticles can cause DNA damage to developing brain cells when exposed to cellular barriers. This damage is dependent on astrocytes and has implications for the development of potential drug targets in treating neurodegenerative conditions.
New research reveals how alcohol causes permanent genetic damage to blood stem cells, leading to cancer. The study found that acetaldehyde breaks and damages DNA within these cells, altering chromosome sequences and increasing the risk of certain cancers.
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Researchers found that low-dose X-ray treatment does not induce genome instability or DNA damage in stem cells. Instead, these cells proliferate and maintain their health, contradicting previous assumptions about the harm caused by ionizing radiation.
A diabetes drug has been found to improve DNA repair in cells affected by Xeroderma pigmentosum, a rare genetic disease. The drug, acetohexamide, degrades the DNA repair enzyme MUTYH, triggering an NER-independent mechanism for removing UV-induced DNA damage.
Cells can sense and mend damaged DNA caused by certain chemotherapy drugs. Researchers discovered a previously unknown repair complex that targets this type of damage. This finding could lead to more effective chemotherapy treatments by amplifying the killing power of existing drugs.
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Researchers at Osaka University have discovered a key role for protein SCAI in selecting between DNA repair mechanisms, NHEJ and HR, in response to damage. The study found that SCAI promotes the recruitment of HR proteins by binding to 53BP1.
A new study reveals that tadpoles living in low-temperature environments are more susceptible to DNA damage from UV radiation. This increased risk can lead to mutations and cell death, contributing to the global amphibian extinction crisis.
Astronauts are exposed to DNA damage due to zero gravity and cosmic radiation; an automated diagnostic procedure is being adapted for use in space, promising constant conditions for each sample. The device could also be used to evaluate the effects of radiotherapy.
Research suggests that night shift work impairs the body's ability to repair DNA damage caused by normal cellular processes. Suppression of melatonin, a hormone regulating the internal clock, is thought to be a key factor in this impairment. This may result in higher levels of DNA damage and potentially carcinogenic effects.
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A study by the University of East Anglia warns that common water treatments containing colloidal silver may cause genotoxicity, damaging DNA. This can lead to reproductive issues and harm to future generations. The World Health Organization advises against its use as a primary water treatment.
New research reveals the role of enzyme-catalyzed decomposition in the antitumor effect of oxazaphosphorines. Activated oxazphosphorines are decomposed into phosphoreamide mustard and 3-hydroxypropanal, causing DNA damage that can lead to apoptosis.
A UConn study uses a novel device to detect DNA damage caused by e-cigarette vapor, finding that non-nicotine e-liquids can also cause DNA damage similar to filtered cigarettes. The researchers' findings raise concerns about the potential health risks of e-cigarettes.
A new technique developed by UNC School of Medicine scientists has mapped DNA damage caused by cigarette smoking at high resolution across the genome. The study provides a genome-wide map of the damage caused by benzo[α]pyrene, a chemical that accounts for about 30 percent of cancer deaths in the United States.
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A CU Boulder study shows that some dividing human cells transmit low-level DNA damage to their daughters, causing them to enter a quiescent state previously thought to be random. The process is linked to the fate of daughter cells in subsequent cell cycles and has implications for cancer development and aging.
Researchers at the University of Maryland School of Medicine found that CHD4, a protein that usually prevents mutation, can become a protector of cancer cells. The protein plays a key role in DNA damage repair and may be linked to cancer progression.
Ben-Gurion University researchers found that SIRT6 protein levels are significantly lower in Alzheimer's patients and contribute to the onset of the disease. The study suggests a link between low SIRT6 levels and DNA damage accumulation, which may lead to neurodegenerative diseases.
Researchers at Johns Hopkins Kimmel Cancer Center discover that cancer cells hijack the DNA repair machinery to sustain their growth. By inhibiting this mechanism, they found potential targets for anticancer drugs and ways to track cancer recurrence.
A new study sheds light on the dark side of tumor suppressor gene p53, revealing that regulating genes Mdm2 and Mdm4 keep mutated p53 in check. The study shows that mutating these proteins can lead to an elevation of mutant p53, driving cancer growth.
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