Dna Repair
Articles tagged with Dna Repair
Researchers find potential one-two punch against triple-negative breast cancer
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.
Scientists discover a new way to make drug-resistant cancer treatable again
Researchers discovered a small molecule, UNI418, that destabilizes key DNA repair proteins, making drug-resistant cancer cells vulnerable to PARP inhibitor therapy. This approach restores tumor sensitivity and improves treatment outcomes.
Best snapshots yet of DNA repair protein relevant to BRCA mutations
Researchers have captured the most detailed structural images to date of a specific type of protein's DNA repair process, revealing key steps in its repair activities. The findings provide insights for drug targets that could halt the process in cancer cells empowered by mutated BRCA genes.
A new view of aging: How the immune system rewrites rapid aging
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.
Gene–phenotype catalogue provides new insights into premature aging disorders
A new gene catalogue provides comprehensive insights into premature aging disorders, highlighting the central role of genome maintenance and DNA repair pathways. The catalogue organizes genetic and clinical information for 56 syndromes and 160 distinct clinical entities, offering a valuable framework for future research.
Study: Blocking a key protein may create novel form of stress in cancer cells and re-sensitize chemo-resistant tumors
A new study suggests blocking key protein p300 can create novel form of cellular stress in cancer cells, re-sensitizing chemo-resistant tumors. Cells produce proteins even with damaged DNA, leading to toxic buildup and stress inside the cell's internal quality-control system.
Five mutational “fingerprints” could help predict how visible tumours are to the immune system
Researchers discovered five dominant patterns of protein-altering mutations that determine tumor visibility to the immune system. These 'fingerprints' help predict immunotherapy response and suggest a more personalized approach to cancer treatment.
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.
Eye for trouble: Automated counting for chromosome issues under the microscope
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.
Scientists find cancer weak spot in backup DNA repair system
Researchers discovered that certain cancers rely on an emergency DNA repair mechanism called break-induced replication to survive. By understanding how this mechanism works, scientists can develop targeted therapies to selectively kill cancer cells while leaving normal cells intact.
Experimental drug repairs DNA damage caused by disease
Scientists have developed an experimental drug called TY1 that repairs DNA damage and promotes healing in damaged tissue. The breakthrough could lead to new treatments for heart attacks, autoimmune diseases, and other conditions.
DNA shape and rigidity regulate key players of gene expression
Researchers at the University of Texas M. D. Anderson Cancer Center discovered that inflexible DNA within nucleosomes regulates the positioning of INO80, a chromatin remodeling complex. This unique mechanism allows INO80 to position itself on the surface of nucleosomes at the right location.
Study uncovers hidden class of BRCA1 mutations and a potential way to target them
Researchers have discovered a new class of BRCA1 mutations that can be targeted by HSP90 inhibitors, potentially improving treatment outcomes for patients with breast cancer. The study found that these mutations are more resistant to PARP inhibitor treatment but can be overcome with low-dose HSP90 inhibition.
New type of DNA damage found in our cells’ powerhouses
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.
Dicer: Life's ancient repair tool
A team of scientists has found that Dicer, an ancient protein, plays a vital role in resolving conflicts between transcription and replication processes in the genome. Without Dicer, T-R collisions lead to DNA damage, mutations, and cancer. The study highlights the importance of Dicer in maintaining genome stability.
Hunting for the chromosomal genes that break the heart
Researchers used CRISPR technology to identify HMGN1, a nuclear binding protein that contributes to trisomy 21-related CHDs. The study found that an overabundance of HMGN1 leads to abnormal heart development and gene expression.
New research reveals genetic link to most common pediatric bone cancer
Researchers identified a previously unknown gene, SMARCAL1, that increases the risk of developing osteosarcoma in children and young adults. The study found that approximately 2.6% of children with osteosarcoma carry inherited mutations in SMARCAL1, which may weaken DNA repair and promote tumor growth.
CNIO researchers create the “human repairome”, a catalogue of DNA “scars” that will help define personalized cancer treatments
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.
Does early-life cellular activity influence cancer and aging?
Telomeres, which cap chromosomes, are inherited from parents in a parent-of-origin effect, with mothers contributing short telomeres and fathers long ones. This process is linked to cancer risk and aging, and researchers hope to study it further using human genome sequencing.
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.
Enzyme protects developing brain from harmful mutations
A recent study by researchers at The University of Osaka discovered the crucial role of DNA repair enzyme Polβ in safeguarding the developing brain from harmful mutations. Accumulation of indel mutations near CpG sites may contribute to neurodevelopmental disorders.
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.
How DNA packaging controls the “genome’s guardian”
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.
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.
Association for Molecular Pathology publishes best practice recommendations for clinical HRD testing
The Association for Molecular Pathology publishes guidelines for detecting homologous recombination deficiency (HRD) in cancer. The report includes recommendations for clinical laboratories, addressing technical aspects of genomic instability and HRD analysis.
MD Anderson Research Highlights for June 11, 2025
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.
Cigarette smoke and DNA repair deficiency drive lung cancer development
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.
Study reveals intricate molecular detail of human DNA repair process
Researchers have revealed the structural mechanisms of a major DNA repair pathway in human cells, showing how RAD51 filament promotes strand exchange and facilitates DNA repair. The study provides fundamental insights into biochemical reactions of eukaryotic homologous recombination.
Scientists discover potential new targets for Alzheimer’s drugs
Scientists at MIT have identified new potential targets for treating Alzheimer's disease, including a pathway involved in DNA damage repair. The study suggests that a combination of treatments targeting different cellular pathways may be more effective in blocking disease progression.
“Cutting to survive”: how cells remove DNA bridges at the last moment
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.
A more realistic look at DNA in action
Researchers at Northwestern University discovered that DNA's behavior changes in a crowded environment, affecting the amount of stress required for strand separation. The study used microscopic magnetic tweezers to investigate interactions between DNA and various molecules.
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.
Light bulb moment for understanding DNA repair switches
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.
Unexpected protein structure may lead to new cancer treatments
A University of Iowa-led study has revealed the unexpected structure adopted by the DNA repair protein RAD52 as it binds and protects replicating DNA in dividing cells. This understanding may help researchers develop new anti-cancer drugs targeting RAD52.
Cellular circuit controls how DNA damage is repaired, affecting risk of disease as we age
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.
Research by UMass Chan scientists upends scientific understanding of how anticancer drugs kill cancer
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.
How a crucial DNA repair protein works—and what it means for cancer treatment
Researchers at Scripps Research have captured the first detailed images of polymerase theta (Pol-theta) in action, revealing its molecular processes responsible for a range of cancers. The study provides a blueprint for designing more effective cancer drugs by understanding how Pol-theta repairs DNA using a two-step process.
Radiotherapy impacts survival differently in glioblastoma and low-grade glioma
A new study reveals that radiotherapy has opposite effects on glioblastoma multiforme (GBM) and low-grade gliomas (LGG), with GBM patients living longer after treatment. The study highlights the need for personalized treatment approaches based on genetic and molecular characteristics to improve survival outcomes.
Antiviral protein causes genetic changes implicated in Huntington’s disease progression
Research suggests that APOBEC enzymes, which normally target viruses, are unusually active in the brains of Huntington’s patients and cause genetic changes. The study found that APOBEC3A was most pronounced in causing DNA repeat expansion in a CAG/CTG tract.
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 CRISPR toolkit to allow remote-controlled genome editing
Engineers at USC Viterbi School of Engineering have developed a new CRISPR toolkit that allows for precise, remote-controlled genome editing using focused ultrasound. This breakthrough enables the treatment of various genetic disorders and diseases by activating or silencing specific genes with precision.
DNA repair: A look inside the cell’s ‘repair café’
Researchers at the Hubrecht Institute have mapped the activity of DNA repair proteins in individual human cells, discovering unique and sometimes rare ways to repair DNA damage. These proteins organize into 'hubs' where multiple damaged DNA regions come together, making the process more efficient.
University of Oregon researchers unravel how a breast cancer gene affects fertility
Researchers have uncovered a mechanism by which the BRCA1 gene influences fertility, leading to genetic errors that can cause infertility. This breakthrough discovery enables potential therapeutic avenues for correcting or treating fertility issues in BRCA1 patients.
UT Health San Antonio-led study finds novel role of BRCA1 in tumor suppression
A new study by UT Health San Antonio reveals that BRCA1 plays a crucial role in promoting error-free DNA repair through the activation of end resection enzymes. This understanding sheds light on the tumor suppressor function of BRCA1 and has important implications for breast and other cancers.
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.
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.
Shedding light on the mechanism of yeast DNA repair
Researchers investigated the central role of Sae2 in regulating yeast DNA repair. A recent study found that Sae2 controls Mre11 endo- and exonuclease activities via different mechanisms, essential for maintaining genetic information.
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.
ERC Advanced Grant for Helle Ulrich for research on DNA repair and genome stability
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.
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.
Pacific Northwest Research Institute uncovers hidden DNA mechanisms of rare genetic diseases
Researchers at PNRI reveal how specific DNA rearrangements called inverted triplications contribute to the development of various genetic diseases. These complex rearrangements are caused by segments of DNA switching templates during the repair process, leading to disruptions in normal gene function and contributing to genetic disorders.
Synergistic cytotoxicity of HDAC and PARP inhibitors and decitabine in pancreatic cancer cells: implications for novel therapy
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.
Engineered DNA 'warhead' targets a common cancer mutation
A team of researchers from Xi'an Jiaotong-Liverpool University has engineered a short sequence of artificial DNA to target the mutant protein p53-R175H, linked to lung, colorectal, and breast cancers. The new molecule, dp53m, inhibits cancer cell growth and increases sensitivity to chemotherapy agent cisplatin.
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.
Cockayne syndrome: new insights into cellular DNA repair mechanism
Researchers have uncovered important details about the role of CSB/ERCC6 and CSA/ERCC8 genes in Cockayne syndrome. These genes encode enzymes associated with DNA repair that initiate transcription-coupled repair of toxic DNA-protein crosslinks, marking and breaking down damaged DNA.
How a natural compound from sea squirts combats cancer
Researchers have deciphered trabectedin's precise mechanism of action, revealing its ability to induce persistent DNA breaks in cancer cells. This disruption of the transcription-coupled nucleotide excision repair (TC-NER) pathway leads to long-lasting DNA breaks that ultimately kill cancer cells.
Making ends meet: Researchers find that a protein superglue is crucial for DNA damage repair
A protein called PARP1 forms a special healing zone that holds loose DNA ends together and allows DNA repair to begin. This discovery provides valuable insight into the molecular basis of DNA damage repair and its potential application in cancer treatment.
Scientists unravel key steps in the road to DNA repair
Researchers have discovered that RecA protein repairs breaks in double-stranded DNA without unwinding the helix, leading to a new understanding of homologous recombination. This breakthrough has significant implications for breast cancer research and may lead to new treatments.