Articles tagged with Dna Damage
Researchers analyzed over 600 tumors from 544 patients and found distinct genomic signatures of DNA changes linked to different chemotherapies. These patterns appeared as early as 91 days after treatment began, allowing clinicians to track treatment-resistant tumours and potentially reduce toxic effects. The study could lead to a more ...
Researchers at Wayne State University and Indiana University have developed a new class of drugs that target the Ku70/80 DNA-binding complex, a critical enzyme in DNA damage response. This approach aims to sensitize cancer cells to radiation and improve radiotherapy outcomes for lung cancer patients.
Researchers developed a human-safe drug that repairs DNA breaks and reduces inflammation in a mouse model of Alzheimer's disease. The approach targets multiple disease-relevant cellular pathways, providing a broader therapeutic strategy than previous approaches focused on individual disease hallmarks.
Scientists at King's College London have developed a human-safe drug that repairs DNA breaks and reduces inflammation in a mouse model of Alzheimer's disease. This approach targets multiple features of the disease simultaneously, providing a broader therapeutic strategy than previous approaches focused on individual disease hallmarks.
Australian researchers found short bursts of intense UVB radiation caused 50% more DNA damage in tadpoles than a lower level for a longer period. This type of damage could impact frog growth and survival.
A new study reveals that p38MAP kinase plays a central role in regulating senescence-related changes in human muscle cells. The researchers developed a human cell-based model to investigate how senescence develops in skeletal muscle cells and identified a signaling pathway that appears to drive aging in mature muscle fibers.
Researchers at Niigata University have uncovered a new function of APP, promoting lysosomal exocytosis to expel damaged nuclear material and protect neurons from damage. Reduced APP levels or mutations associated with familial AD led to accumulation of nuclear waste, triggering neuroinflammation and cell death.
Researchers found a unique protein called YAF9B that helps plants protect their stem cells from DNA damage. This discovery sheds light on how plants coordinate DNA repair processes, which could improve future crops by guiding more precise genome editing.
Researchers from Florida Atlantic University have identified a key immune pathway that appears to drive damaging inflammation in Huntington disease. Blocking this pathway reduced brain inflammation, protected neurons, and improved movement in a humanized mouse model of the disease.
Researchers at the University of Pittsburgh School of Medicine discovered an unexpected chromosome interaction between telomeres and centromeres in some aggressive cancers. This interaction creates a genetic signature that could help identify ALT-positive tumors, which are often challenging to treat due to genomic instability.
Researchers discovered a fast protective mechanism in cells that forms a ring-like structure around the nucleus to prevent DNA damage and cell death. This 'actin ring' protects the nucleus by confining and stabilizing it, making it less likely to rupture.
Researchers discovered that overproduction of a DNA repair protein creates DNA damage mimicking BRCA mutations, which may respond to targeted treatments. Tumors with high levels of EXO1 protein exhibit characteristics similar to BRCA-mutant cells, suggesting personalized therapies could be effective.
A new study reveals that the cancer-causing protein MYC plays a direct role in fixing damaged DNA in tumor cells. This allows cancer cells to survive chemotherapy and other treatments, contributing to tumor resistance and poor patient outcomes. The findings could lead to new therapies targeting MYC's repair function.
Researchers developed RegVelo, an AI framework that models cellular dynamics and gene regulation to predict cellular fate decisions. The model traces developmental trajectories and simulates regulatory interactions, providing insights into hidden drivers of development and potential therapeutic targets.
Researchers found that DNA helicase HELQ promotes replication fork reversal to protect cells from toxic DNA crosslinks. This process enables stalled replication forks to reverse and stabilize, minimizing mutations and cell death. The study identifies HELQ as a critical regulator of genome integrity under replication stress.
A new CRISPR protein, Cas12a2, has shown potential for killing sick cells while leaving healthy ones untouched. Researchers have tested its effectiveness in destroying cancer cells and virus-infected cells with promising results.
Researchers at UT MD Anderson Cancer Center have made significant advancements in targeted therapy treatments for advanced lung cancer and early-stage classical Hodgkin lymphoma. The studies showcase high response rates with novel combination therapies and a new understanding of how an enzyme affects infertility and cancer progression.
A study published in Cell Reports Medicine found that inhibiting RNase H2 can cause significant damage to DNA and activate the innate immune system to produce signals that attract T cells to attack the tumor. This approach could lead to improved patient outcomes for patients with triple-negative breast cancer.
Researchers developed RF-SIRF, a quantitative method to detect and map reversed DNA replication forks with single-cell resolution. The study identified unique epigenetic codes for DNA replication stress that can be further examined to understand genomic stability, aging, and treatment response.
Researchers at Tohoku University discovered a hidden mechanism in DNA damage caused by singlet oxygen generating abasic sites. This process is common and represents one of the main forms of DNA damage, alongside guanine-related types.
Researchers identified the misdirected immune response as a central driver of tissue degeneration in severe, rapid-aging disorders. By reducing this false alarm, they restored function across multiple biological systems, suggesting the body can cope with more DNA damage than assumed if inflammation is kept in check.
A new blood-based biomarker has been discovered to help identify individuals at higher risk of developing cancer in people with Lynch Syndrome. The biomarker uses immune signatures detected in blood samples to provide unique characteristics that can detect cancer risk, allowing for early detection and personalized surveillance.
The project aims to test whether reducing chronic inflammation triggered by DNA can help older adults stay healthier. The research focuses on retrotransposons, which become increasingly active with age, leading to tissue decline.
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.
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.
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 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.