Dna Damage Responses
Articles tagged with Dna Damage Responses
UT MD Anderson shares latest research breakthroughs
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.
Scripps Research scientists uncover new mechanism cancer cells use to survive DNA damage
Researchers uncover a new way cancer cells repair broken DNA at replication forks, allowing them to survive relentless replication stress. This discovery reshapes understanding of how tumor cells repair DNA and suggests that blocking a key enzyme may be an effective strategy to selectively target cancer.
Researchers identify blood-based biomarker for cancer risk in people with Lynch Syndrome
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.
A broken DNA repair tool accelerates aging
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.
New study uncovers how DNA damage can lead to Motor Neurone Disease
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 uncover new way in which cells tolerate anticancer drugs
Researchers found that Fen1 protein improves cell tolerance to alovudine by counteracting the toxic effect of 53BP1. This discovery promises new cancer treatments and biomarkers for cancerous cells with Fen1 deficiency.
Chemical shield stops stressed DNA from triggering disease
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.
New insights into long-term dysfunction of edited blood stem cells and how to overcome it
Scientists at San Raffaele Telethon Institute for Gene Therapy discovered that CRISPR-Cas9 gene editing can cause inflammation and senescence-like responses in blood stem cells. This reduces the cells' ability to regenerate blood cells after transplantation, limiting the long-term success of gene therapy.
Inhibiting ADAM19 reduces gut inflammation and cell aging markers across species
Researchers have discovered that inhibiting the metalloprotease ADAM19 can reduce gut inflammation and cell aging markers across species. The study found that blocking ADAM19 reduced gut damage and inflammation in fruit flies, mice, and human cells, offering a promising path for creating treatments to maintain healthy tissues.
Researchers reveal reciprocal interaction between extrachromosomal DNA maintenance and DNA damage response
A research team has uncovered a reciprocal regulatory relationship between extrachromosomal DNA maintenance and the DNA damage response in tumor cells. The study found that ecDNA actively replicates and is stably maintained in ecDNA-positive cells, triggering the ATM-mediated DDR pathway.
AACR: First-in-class covalent Werner helicase inhibitor shows clinical proof-of-concept in Phase I trial
The treatment demonstrated early signals of efficacy, with 65.7% of patients experiencing lasting stable disease, and was generally well-tolerated, with most adverse events being mild and manageable.
Stephen Hauser wins breakthrough prize for role in redefining MS
Neuro-immunologist Stephen Hauser has won the 2025 Breakthrough Prize in Life Sciences for his role in identifying the immune system's primary driver of damage to nerve cells in multiple sclerosis. His B-cell theory has led to the development of therapies that have transformed treatment, reducing relapses and improving prognosis.
Chinese Medical Journal article reveals the anticancer potential of poly ADP-ribose polymerase inhibitors
PARP inhibitors have been found to be effective in treating cancers with BRCA1/2 mutations by blocking DNA repair pathways. The combination of PARPis with chemotherapeutic drugs can also improve treatment efficacy, increasing DNA damage and blocking repair processes.
A protein from tiny tardigrades may help cancer patients tolerate radiation therapy
Researchers have developed a new strategy to protect cancer patients from radiation-induced DNA damage using a protein from tardigrades. The approach makes use of messenger RNA encoding the protein, which is delivered to patient tissues before radiation treatment. This reduces double-stranded DNA breaks by 50% in mouse models.
Completely different mechanisms cause damage in males and females with a rare genetic syndrome
Researchers found that a rare genetic syndrome causes different damage mechanisms in male and female brains, affecting neurogenesis and energy production. The study suggests that the ADNP protein plays a crucial role in brain development and aging, with distinct functions in males and females.
Chinese Medical Journal review highlights senescence’s dual role in liver disease and emerging therapies
Researchers reveal senescence's impact on liver health, from repair and regeneration to chronic disease progression. Emerging therapies, such as senolytic treatments, aim to selectively eliminate senescent cells while preserving healthy tissue.
Textbooks need to be rewritten: RNA, not DNA, is the main cause of acute sunburn
Researchers found RNA damage triggers inflammation and cell death in skin after UV exposure. The ribotoxic stress response, orchestrated by protein ZAK-alpha, plays a key role in this process.
Mystery solved: how tumor cells die after radiotherapy
Researchers discovered that DNA repair determines how cancer cells die following radiotherapy, with specific pathways triggering cell death noticed by the immune system. Blocking these pathways can force cancer cells to die in a manner that alerts the immune system, leading to new potential treatments.
New mechanism discovered that triggers immune response in cells with damaged DNA
UC Irvine researchers have identified a previously unknown mechanism that triggers an inflammatory immune response in cells with damaged DNA. This discovery may lead to more effective cancer treatments by allowing doctors to personalize therapies tailored to individual patients' needs.
Cancer’s reach across the animal kingdom
A comprehensive study examining over 16,000 necropsy records from 292 vertebrate species found significant differences in cancer prevalence. Cancer rates increase with body size and cellular mutation rates but decrease with longer gestation periods.
Researchers offer alternative to hydroxyurea in study of DNA replication process
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.
Study finds common breast cancer treatments may speed aging process
A new study found that common breast cancer treatments, including chemotherapy, radiation, and surgery, can increase expression of aging markers in breast cancer survivors. The study suggests that these treatments can have a more extensive impact on the body than previously thought, leading to accelerated biological aging.
How cells recognize and repair DNA damage
A new mechanism of DNA damage response has been identified, involving an RNA transcript that regulates genome stability. The study found that NEAT1, a long non-coding RNA transcript, plays a crucial role in recognizing and repairing DNA double-strand breaks.
NTU Singapore and Oxford study discover new process for cells to repair DNA damage
Researchers at NTU Singapore and Oxford have identified a new process called nucleophagy that helps cells remove harmful DNA-protein lesions, promoting genetic material stability and cell survival. This discovery may improve cancer treatment outcomes for patients with colorectal cancer.
2-bromopalmitate reduces senescence in human cells: Role of palmitoylation
A new study found that 2-bromopalmitate treatment reverses cell senescence in human vascular smooth muscle cells, reducing DNA damage markers and promoting cell proliferation. The research suggests a critical role for protein palmitoylation in regulating the senescent phenotype.
Demystifying APE1: New findings on direct activation of ATM signaling by DNA single-strand breaks
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.
UV radiation damage leads to ribosome roadblocks, causing early skin cell death
A recent study by Johns Hopkins Medicine reveals that the ZAK protein is a critical player in the cell's response to UV radiation damage, determining whether cells live or die. The research, published in Cell, suggests that companies developing drugs targeting ribosomes may find ZAK to be a driver of cell death across cancer types.
Starving cancer cells to enhance DNA damage and immunotherapy response
Researchers at Howard University have identified a new therapeutic strategy to combat prostate cancer by depleting amino acids. This depletion induces oxidative stress and DNA damage in cancer cells, making them more susceptible to treatment with DNA repair-targeted and immune checkpoint blockade therapies.
How E. coli defends itself against antibiotics
When E. coli detects damage from antibiotic Ciprofloxacin, it sends out an SOS signal that alters cellular activity. The bacteria then mutate their DNA to repair the damage or adapt to resist the antibiotic. Researchers studied this process in detail using bioreactors and found all genes are activated simultaneously at the protein level.
Germline regulation and sex differences: How they impact lifespan in vertebrates
A new study reveals sex-specific effects of germline regulation on longevity and somatic repair in vertebrates. Removing the germline extends male lifespan and improves stress resistance in females.
How aging clocks tick
Scientists have discovered that aging clocks measure stochastic changes in cells, rather than damage accumulation. This finding suggests that aging can be predicted using the variation in cellular processes.
Transfected SARS-CoV-2 spike DNA suppresses cancer cell response to chemotherapy
Researchers found that SARS-CoV-2 spike protein interrupts p53-MDM2 interaction but does not bind with p53 protein in cancer cells. The study also shows that SARS-CoV-2 spike suppresses p53-dependent gene activation, leading to increased cell viability after chemotherapy exposure.
Toronto researchers uncover human DNA repair by nuclear metamorphosis
Researchers at the University of Toronto have discovered a DNA repair mechanism that uses nuclear metamorphosis to fix double-strand breaks in human cells. This discovery has significant implications for cancer treatment and premature aging, and may lead to new therapeutic avenues.
UNC-Chapel Hill researchers discover new clues to how tardigrades can survive intense radiation
Researchers at UNC-Chapel Hill have found that tardigrades can increase DNA repair genes' production in response to radiation, making them more resilient to damage. This discovery could lead to new ideas on protecting other animals and microorganisms from damaging radiation.
Impact of aldehydes on DNA damage and aging
Researchers at Nagoya University discover aldehydes cause DNA damage and contribute to premature aging in humans. The team proposes a link between aldehyde-derived DNA damage and premature aging, highlighting potential targets for therapeutic intervention.
Longer genes are linked to aging
Four studies conclude that longer genes are most susceptible to aging due to increased potential sites for DNA damage. Long genes have more sites for damage, making them prone to degradation with age, contributing to conditions like Alzheimer's disease.
PR55α-controlled PP2A Inhibits p16 Expression and Blocks Cellular Senescence Induction
Researchers have discovered that PR55α, a regulatory subunit of PP2A phosphatase, inhibits p16 expression and blocks cellular senescence induction by γ-irradiation. This finding provides a new insight into the regulation of the p16/RB pathway in response to stressors.
Some tumors ‘grow bad’: Why a dangerous subtype of Wilms tumor is so resistant to chemotherapy
A team of researchers found that diffuse anaplasia (DA) subtype of Wilms tumor grows despite high DNA damage and TP53 mutation, leading to resistance to chemotherapy. The study suggests that DA histology emerges through accumulating DNA damage and CNAs, creating selection pressure for TP53 mutations.
ATR inhibition using gartisertib in patient-derived glioblastoma cell lines
Researchers identified gartisertib as a potent ATR inhibitor that enhances cell death in patient-derived glioblastoma cell lines. The study also showed synergy between gartisertib and TMZ+RT treatment, with higher sensitivity to gartisertib observed in MGMT promoter unmethylated cells.
Protein complex discovered to control DNA repair
A team of scientists has identified a previously unrecognized control point in DNA repair processes, which could lead to novel cancer therapies by inhibiting the repair of damaged cancer cells. The newly discovered GSE1-CoREST complex contains three enzymes that control DNA repair and may form the basis for improved cancer treatments.
Scientists find “key” to potential breast cancer prevention, treatment
Researchers have found that a specific pathway, cGAS-STING, is unleashed to prevent cancer formation by detecting DNA damage within cells. The discovery reveals the 'key' to unleashing this pathway, which can potentially reactivate it to treat and prevent breast cancer development.
Could a drug prevent hearing loss from loud music and aging?
Researchers have identified a gene that links deafness to cell death in the inner ear, creating new opportunities for preventing hearing loss. The discovery suggests that UPR-blocking drugs could prevent deafness caused by loud noise exposure or aging.
Sirtuin 6 activation rescues the age-related decline in DNA damage repair in chondrocytes
This study found that SIRT6 activation improves DNA damage repair efficiency and reduces baseline DNA damage in chondrocytes from older donors. MDL-800 treatment also lowered p16 promoter activity and decreased DNA damage in murine cartilage explants, supporting the concept of SIRT6 as a critical regulator of DNA repair.
Repairing nerve cells after injury and in chronic disease
Researchers at Salk Institute uncover a mechanism for repairing damaged nerves during peripheral neuropathy, with protein Mitf playing a key role. The findings have the potential to inspire novel therapeutics that bolster repair function and heal peripheral neuropathy.
Scientists discover a new stress response pathway for repairing RNA-protein crosslinks caused by toxic aldehydes
Researchers have identified a new mechanism for removing RNA-protein crosslinks induced by aldehydes, which can damage cellular function. This discovery sheds light on the effects of aldehydes on human cells and may be particularly important for maintaining cell function in older individuals.
Key clues to DNA repair mechanism might lead to new cancer treatments
Researchers identified key factors in DNA repair, revealing the 'proofreading' portion of polymerase epsilon helps prevent strand breakage. This knowledge arms scientists with ways to enhance anti-cancer drug effectiveness and develop new diagnostic methods.
Human Lung Chip leveraged to faithfully model radiation-induced lung injury
Researchers developed a human in vitro model of radiation-induced lung injury, closely mimicking the complexities of the disease. The Human Lung Alveolus Chip recapitulates hallmarks of RILI, including DNA damage, inflammation, and injury to lung cells and blood vessels.
New specimen collection system enhances assisted reproductive technologies
A new specimen collection system has been developed to enhance assisted reproductive technologies by providing a simple one-step method for selecting high-quality sperm for ICSI. The system, known as NovaSort, uses a barrier mesh to isolate mobile sperm without damaging their DNA.
Better together against cancer
Researchers combined three highly potent cancer drugs in a single prodrug that is activated in tumor cells, resulting in improved efficacy and reduced side effects. The new approach has shown promise as a potential solution to reduce the burden on patients' bodies during cancer treatment.
DNA damage-induced senescence model in osteoarthritic chondrocytes
Researchers developed a DNA damage-induced senescence model in osteoarthritic chondrocytes, which reliably induces cellular senescence and accumulates senescent cells in OA joint tissues. The study provides a useful model to develop therapeutic approaches targeting senescence in osteoarthritis.
Newly discovered fungus helps destroy a harmful food toxin
A newly discovered fungus has been found to transform the toxic compound patulin into less harmful byproducts, offering potential solutions for controlling its presence in food products. The fungus, identified as Acremonium sp., was shown to degrade patulin into desoxypatulinic acid and other compounds, which are significantly less toxic.
The oldest and fastest evolving moss in the world might not survive climate change
The oldest and fastest evolving moss in the world, Takakia, may not survive climate change. Despite its rapid adaptation capabilities, the species is declining in population size due to warming temperatures and increasing UV radiation, threatening its very existence.
Male germ cells are mainly responsible for gene changes
Research by Professor Björn Schumacher investigates the role of male germ cells in genetic mutations. The study suggests that paternal DNA damage can lead to faulty repairs in the genome, resulting in structural variants.
DNA damage repaired by antioxidant enzymes
The nucleus is metabolically active and uses antioxidant enzymes to repair DNA damage. Cells relocate mitochondrial machinery to the nucleus in response to DNA damage, highlighting a paradigm shift in cellular biology.
How DNA repair can go wrong and lead to disease
A study by Tufts University researchers reveals how DNA repair can fail near expanded repeats, leading to mutations and disease. The team found that certain proteins play a crucial role in stabilizing the DNA during repair.
Hanging on for dear life
Researchers at Tokyo Medical and Dental University identify a novel focal adhesion remodeling process that strengthens cell-matrix adhesion in response to genotoxic stress. This mechanism involves the replacement of FAK with FRNK, leading to increased firm cell attachment.
Genes & Cancer | VCP/p97 as a therapeutic target in KRAS-mutant pancreatic cancer
Researchers have found that valosin-containing protein (VCP) is essential for KRAS-mutant pancreatic ductal adenocarcinoma cell growth and survival. Inhibiting VCP, combined with autophagy inhibition, enhances efficacy in preclinical studies.
Researchers highlight nucleolar DNA damage response in fight against cancer
Scientists from the University of North Carolina at Charlotte review nucleolar DNA damage response pathways to combat cancer. By attacking these mechanisms, researchers aim to disrupt cancer's reproduction and growth.
Scientists observe “quasiparticles” in classical systems for the first time
Researchers at Ulsan National Institute of Science and Technology (UNIST) have observed quasiparticles in a classical system made of microparticles driven by viscous flow. The hydrodynamic forces among the particles create pair excitations that propagate through the crystal, stimulating the creation of new pairs.