Articles tagged with Dna Damage
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A Goethe University-led study reveals how mutations in the SPRTN enzyme cause chronic inflammation and premature ageing. The research team found that damaged DNA in the cell nucleus leaks into the cytoplasm, activating defense mechanisms and leading to chronic inflammation.
A machine-learning-based algorithm developed by Tokyo Metropolitan University researchers can accurately count sister chromatid exchanges (SCEs) in chromosomes, giving a more objective measurement. The accuracy rate is 84%, which could help diagnose disorders like Bloom syndrome with greater consistency.
A Bar-Ilan University study uncovers the origin of sleep in jellyfish and sea anemones, demonstrating that protecting neurons from DNA damage is a basic function of sleep. The research shows that both species accumulate DNA damage during wakefulness and reduce it during sleep, with increased damage triggering recovery sleep.
Researchers at IIT identified a candidate molecule called Apt1 that enhances existing anticancer therapies by making tumour cells more vulnerable to chemotherapy drugs. The molecule slows DNA repair and impairs the interaction between RAD51 and BRCA2 proteins, inducing synthetic lethality in cancerous cells.
Researchers found that alcohol causes DNA damage, which can lead to cancer, and discovered a repair mechanism using the SXE enzyme complex. Individuals with genetic mutations affecting DNA repair may be more susceptible to alcohol-related cancers.
Research from Florida Atlantic University strengthens evidence that alcohol consumption increases cancer risk, particularly for breast, colorectal, and liver cancers. Higher intake and specific groups, such as African Americans and those with obesity or diabetes, are found to be more vulnerable to the risks.
Researchers discover that CDT1 overexpression suppresses DNA replication and induces DNA damage, potentially leading to genetic mutations and cancer. The study provides molecular insights into the role of CDT1 in cancer development.
Researchers found that DNA loops facilitate homologous recombination, a key DNA repair process linked to cancer. These loops enable the repair machinery to scan for an intact copy of the damaged region more efficiently.
A new type of DNA damage, glutathionylated DNA adducts, accumulates at high levels in mitochondrial DNA, affecting energy production and stress response. The discovery sheds light on how cells sense and respond to stress, with potential implications for diseases like cancer and diabetes.
Researchers developed a new DNA analysis technique to study old genetic samples, shedding light on disease evolution and changes in biology over time. The approach has potential for unlocking the root causes underlying shifting landscapes of modern diseases.
Researchers at CNIO have created a 'human repairome', a catalogue of 20,000 DNA 'scars' that reveal how genes affect DNA repair. This information can help determine the best treatment for each cancer type and overcome resistance to therapy.
Research by University of Pittsburgh scientists discovered that damaging telomeres can lead to dysfunctional T cell function. To combat this, they developed a targeted antioxidant approach that rescued T cell function, opening the door for novel therapies in cancer immunotherapies.
A nationwide biomonitoring study in China detected 25 primary aromatic amines with varying levels of exposure among residents. High concentrations were observed in smokers, non-adults, and industrialized cities, with correlations to oxidative DNA damage.
Researchers found that mutations in the CFAP410 gene change its interaction with another protein, making motor neuron cells more vulnerable to DNA damage and cell death. This discovery provides new insights into the mechanisms underlying Motor Neurone Disease and highlights potential targets for new therapies.
Scientists have developed a new method to visualize and analyze the complex shapes of DNA molecules using atomic force microscopy. This breakthrough enables researchers to study the tangled structures of DNA in cells, which can lead to insights into diseases such as cancer and neurodegeneration.
Scientists have found that nucleosomes act as gatekeepers for p53's molecular partners, controlling its access to the genetic code. This discovery reveals a new layer of regulation over p53's activity and opens possibilities for developing cancer therapies that restore or control p53 function.
Researchers developed a chemical probe that binds to damaged mitochondrial DNA, blocking enzymatic processes that lead to its degradation. This approach lessens mtDNA loss, preserving energy production in vulnerable tissues. The new molecule successfully reduced inflammation and maintained functional DNA despite chemical tagging.
Scientists at UNIGE have identified MLF2 and RBM15 as key proteins regulating chromatin remodelling, which can go awry leading to cancers and neurological disorders. These two proteins could become promising therapeutic targets for diseases linked to disrupted chromatin remodelling.
A new review identifies CHEK2 as a potential biomarker for predicting response to immunotherapy and suggests that combining CHEK2 inhibitors with existing therapies may enhance anti-tumor effects. This could lead to improved treatment outcomes in solid tumors.
Researchers at MD Anderson have made significant progress in treating non-small cell lung cancer (NSCLC) by combining chemotherapy, immunotherapy, and surgery. They found that pre-surgical combination therapy showed promising results, with high rates of pathological complete response and major pathological response.
Researchers found that cigarette smoke and reduced DNA repair capacity combine to increase cancer risk, with normal lung cells showing extensive damage after smoke exposure. The study's findings support a 'double hit' model, highlighting the critical role of XPC protein in preventing DNA damage.
Researchers discovered that blocking PRDX1 protein can make ovarian cancer cells more responsive to DNA-damaging platinum therapies. The study suggests targeting PRDX1 could be a viable strategy to improve chemotherapy efficacy.
A study at the University of Zurich tracks live cellular development and epigenetic changes over multiple generations, showing how stress induces heterogeneity and increases genetic complexity. This research may lead to better understanding of cancer cell diversity and develop more effective therapies.
The microbiome plays a critical role in aging, with dysbiosis accelerating immune decline and systemic diseases. Targeting the microbiome with therapeutic interventions may offer a potent means of extending healthspan.
Researchers have elucidated the molecular mechanism by which LEM-3 cuts DNA bridges during cytokinesis, a crucial step in cell division. The study found that LEM-3 is essential for resolving persistent DNA bridges and maintaining chromosomal stability.
Researchers at University of Seville have discovered patulin and xestoquinol as inhibitors of DNA topoisomerase 1, a key enzyme in DNA metabolism. These natural compounds may provide a new class of anticancer drugs by preventing DNA cuts from being ligated.
Scientists at the University of Birmingham have made strides in understanding how cells repair DNA damage. Two studies identify key players and mechanisms involved in preventing excessive DNA signal overload, which could lead to refinements in future cancer therapies.
Novel biomarkers like miRNA-34a link anthracyclines to cardiotoxicity, while stem cell therapy and nanotechnology offer potential for prevention and treatment. Traditional strategies have limitations, but new approaches hold hope for improved patient outcomes.
A new study led by NYU Langone Health scientists sheds light on how the major cancer gene BRCA2 determines which cancer cells can be killed by a class of precision cancer drugs called PARP inhibitors. Intact BRCA2 functions as a molecular shield, preventing PARP1 from disrupting DNA repair complexes, and its activity dictates PARP inhi...
Senescent cells can cause chronic inflammation through the secretion of inflammatory molecules, leading to age-related diseases. The study found that a cellular circuit controlling DNA repair can suppress this inflammation, offering potential ways to promote healthier aging.
Researchers found that pancreatic cancer cells gain a survival edge by carrying copies of critical cancer genes on circular pieces of DNA outside chromosomes. The discovery highlights the importance of targeting extrachromosomal DNA in treating the disease.
Genetic changes triggered by environmental factors like pollution, diet, and stress can increase cancer risk. Nearly everyone is exposed to cancer risk factors daily, highlighting the need for public awareness and policy action to reduce exposure.
Researchers have discovered a new mechanism of how anticancer drugs attack and destroy BRCA mutant cancer cells, including drug-resistant breast cancer cells. The study found that small DNA nicks can expand into large single-stranded DNA gaps, leading to cell death.
The study reveals that certain DNA regions are more prone to damage but also better repaired by cells. Transcription factors can either help or harm DNA, highlighting the importance of efficient repair in determining mutation formation.
A recent study found that autophagy, a natural defense mechanism in cells, is less efficient in female eggs with moderate or severe DNA damage. Boosting autophagy can improve egg quality and reduce the risk of miscarriage and birth defects. The study's findings offer new directions for improving reproductive health.
A new study identified USP5 as an enzyme crucial for breaking down unneeded or damaged proteins in the heart. Low levels of USP5 lead to protein buildup, triggering dilated cardiomyopathy in animal models. Increasing USP5 levels helps clear protein 'junk', improving heart function and reducing disease progression.
Researchers at King's College London have developed a complex model of molecular 'wear-and-tear' that sheds light on how proteins age. The study found that chromatin, the DNA-protein mix, is more resilient to aging than previously thought, suggesting new avenues for anti-aging treatments.
A systematic review of 24 studies suggests resveratrol can enhance the quantity and quality of egg cells, called oocytes. The compound may also treat infertility related to endometriosis and obesity.
The Neuron special issue sheds light on the science of aging, focusing on how age-related changes impact the brain's ability to clear waste and transport energy. The collection also explores the link between the immune system and brain health.
The study, published in Aging, introduces a new therapy for osteoarthritis that uses extracellular vesicles derived from fat tissue to repair damage caused by aging cells. The treatment showed strong therapeutic effects in both cellular and mouse preclinical studies, reducing inflammation and DNA damage markers in human joint cells.
Researchers have discovered a major setback in the use of AZD7648 to promote precise gene editing, which causes massive genetic changes and genome instability. Despite this, scientists remain optimistic about advancing CRISPR-Cas technology to treat diseases.
A UCI-co-led study found that accumulated DNA damage in the retina contributes to AMD. Targeting specific retinal cell types could lead to treatments that slow or stop progression.
Recent research published in Nature Climate Change highlights the importance of coral reef restoration in responding to smaller-scale disturbances. Leading experts emphasize the need for tailored approaches, incorporating resilience-oriented frameworks to ensure long-term success.
A new study in Addiction Biology suggests that cannabis use can cause chromosomal damage, leading to increased cancer risk and birth defects. This genotoxicity may be transmitted to offspring via damaged sperm or eggs.
Researchers have found that specific E. coli bacteria in the gut promote colon cancer by binding to intestinal cells and releasing a DNA-damaging toxin called colibactin. This binding is made possible by bacterial pili and adhesins, which can be targeted to prevent tumor development.
This study explores the radioprotective effects of Licochalcone B on radiation-induced cell damage and mortality in mice. Lico B significantly improves antioxidant levels, reduces DNA damage, and lowers inflammatory factors.
A new study in mice shows a unique mRNA delivery method can successfully edit faulty genes in fetal brain cells. The technology has the potential to stop progression of genetic-based neurodevelopmental conditions like Angelman syndrome and Rett syndrome before birth.
A new study reveals that benzyl butyl phthalate (BBP) causes oxidative stress and DNA strand breaks, leading to cell death and abnormal chromosomes in egg cells. The research suggests that BBP exposure can lead to lower quality egg cells with compromised genomic integrity.
Polyploidy, a state with extra genetic material, allows cancer cells to survive longer under DNA damage. This phenomenon explains why some cancers are resistant to anti-cancer drug treatments.
Researchers at Colorado State University have identified an alternate method to study changes during the DNA replication process in lab settings using genetically modified yeast. This new approach provides a less toxic and quickly reversible alternative to hydroxyurea, allowing for better insight into cell cycle arrest mechanisms.
A study from Lund University shows that high DNA fragmentation in sperm is associated with doubled risk of preeclampsia and premature birth in women conceived through IVF. The findings suggest that DFI analysis could be used to identify high-risk pregnancies, potentially leading to improved fertility treatment.
A new study found that 5-fluorouracil kills cells by interfering with RNA synthesis, not DNA damage. The findings suggest that combining 5-FU with drugs affecting RNA synthesis could make it more effective in patients with gastrointestinal cancers.
Researchers at Hokkaido University have identified a key gene, glutathione peroxidase 4 (Gpx4), that enables Syrian hamsters to survive extreme cold by limiting cellular damage. The discovery could lead to new treatments for human health, such as improving organ preservation and using hypothermia as a therapeutic tool.
Researchers found that border-associated macrophages (BAMs) with ApoE4 protein produce inflammatory oxygen free radicals, damaging blood vessels. Removing BAMs or reducing ApoE4 expression eliminated the harmful vascular effects. The study may help identify new approaches to preventing or treating Alzheimer's disease.
Researchers discovered that Huntington's disease protein aggregates cause breaks in the nuclear envelope, leading to DNA damage and misregulation of neuronal genes. The study suggests a common mechanism for neurodegenerative diseases involving nuclear aggregate-induced ruptures.
A new Australian study found a strong link between low magnesium levels and high homocysteine, leading to increased DNA damage and susceptibility to Alzheimer's, Parkinson's, gastrointestinal diseases, cancers, and diabetes. Wholegrains, dark leafy vegetables, nuts, beans, and dark chocolate are rich in magnesium.
Researchers have made significant progress in understanding the function of APE1 in DNA damage response, showing that it promotes SSB-induced ATM DDR through two mechanisms. The study provides direct evidence for APE1's active role in activating ATM kinase to promote the repair of single-strand DNA damage.
Professor Helle Ulrich will investigate how a small regulatory protein called ubiquitin contributes to DNA replication and repair, and decipher how cells direct different pathways. The ERC Advanced Grant aims to gain a deeper mechanistic understanding of ubiquitin's function in preventing mutations that can cause ageing and cancer.
Scientists found no significant differences in mutation rates of DNA strands despite different replication processes. The accumulation of mutations is shaped by DNA accessibility on repair efficiency rather than damage location.
A new study found that combining histone deacetylase inhibitors, poly (ADP ribose) polymerase inhibitors, and decitabine resulted in synergistic cytotoxicity in all cell lines tested. This combination impaired DNA repair pathways and altered epigenetic regulation of gene expression.