Articles tagged with Dna Repair Pathways
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.
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.
Researchers uncover Achilles' heel of TMZ chemotherapy resistance, revealing critical insights into mechanisms behind glioblastoma's inactivation of DNA repair pathways. The study sheds light on potential mechanisms of aging and offers new avenues for developing more effective therapies against this devastating cancer.
Researchers at MD Anderson Cancer Center presented findings on novel treatments for MDS, including luspatercept, which significantly reduced the need for blood transfusions in lower-risk patients. Additionally, a triplet therapy regimen improved survival in older adults with FLT3-mutated AML.
The signaling molecule (p)ppGpp regulates diverse cellular processes essential for DNA repair and stress response, enabling bacterial adaptation to adverse conditions. It influences nucleotide excision repair, mismatch repair, and recombinational repair pathways, promoting the survival of bacteria under antibiotic pressure.
Researchers found saruparib to be superior and durable in treating PDX models with BRCA1/2 alterations, outperforming olaparib in terms of complete response rate and progression-free survival. The study's results suggest the promise of PARP1 selective inhibitors as a new therapeutic option for patients with advanced solid tumors.
A KAUST team developed a simple approach to tackle CRISPR's deletion issue by targeting error-prone DNA repair pathways. By modulating specific genes, they reduced large deletions while enhancing homology-directed repair efficiency.
Purdue University researcher Hana Hall explores the role of R-loops in neurodegenerative diseases, including Alzheimer's, by investigating their impact on neuronal aging and DNA damage. Her work aims to understand how R-loop accumulation contributes to cellular stress and damage.
A new study found that PARP1 is involved in the repair of telomeres, which can lead to genomic instability and cancer. Impairing this process can lead to telomere shortening and increased risk of cancer. The findings challenge existing dogma and open up new possibilities for improving cancer therapies.
A UNIGE team has identified the mechanism of action of PARP inhibitors, used to treat breast and ovarian cancer. By blocking one activity while preserving another, these inhibitors can maintain toxic effects on cancer cells while sparing healthy cells.
Researchers analyzed LTBR expression levels in various cancers, finding it associated with low patient survival and immune cell infiltration. The study identified LTBR as a potential target for cancer immunotherapy and marker of poor prognosis.
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.
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.
Researchers unveiled a previously unknown effect of PG545 in ovarian cancer cells, inducing DNA damage and promoting autophagic degradation of RAD51. This breakthrough could aid in selecting the most appropriate treatments for ovarian cancer patients with PARPi resistance.
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.
Researchers at UNC School of Medicine have pieced together the lesser-known DNA repair pathway, polymerase theta-mediated end joining (TMEJ), which is upregulated in patients with hereditary breast cancer, ovarian cancer, and prostate cancer. The discovery could lead to new therapies for cancer by targeting this pathway.
Researchers found that DNA damage accumulates in arteries with aging and contributes to impaired vascular function. In mice lacking or heterozygous for the double-strand DNA break repair protein ATM kinase, aging accelerated vascular dysfunction, including increased arterial stiffness and oxidative stress.
A special supplement presents insights on neurodegenerative diseases, including Alzheimer's and Parkinson's, affecting 55 million people worldwide. Researchers explore novel molecular pathways and therapeutic approaches, such as acupuncture therapy, to alleviate the burden of brain disorders.
Researchers at St. Jude Children's Research Hospital created a more accurate hepatoblastoma model to improve therapies, focusing on DNA damage repair pathways. The model identified potential targets and validated the effectiveness of PRKDC inhibition when combined with doxorubicin, enhancing treatment efficacy.
A new study published in Aging-US has identified the p53-p16/RB-E2F-DREAM complex as a critical regulator of cellular senescence. The researchers found that this complex represses multiple target genes involved in cell cycle regulation, DNA repair, and chromatin structure, leading to the stability of the senescent arrest.
Researchers discovered that MSH2-MSH3 plays a crucial role in selecting the right DNA repair process by interacting with other proteins during DSB repair. This interaction facilitates error-free homologous recombination and blocks error-prone polymerase theta-mediated end-joining.
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.
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.
Researchers used C-trap technology to investigate how different DNA repair proteins identify and bind to their respective forms of damage. They found that some proteins arrived at the damage site together and departed together, while others showed surprising variability in their association and dissociation patterns. The study provides...
A recent study has unveiled how nucleotide excision repair (NER) is controlled at the molecular level, shedding light on its role in cancer treatment. The research revealed that TFIIH uses XPG to stimulate motor activity and locate damaged DNA, licensing XPG nuclease activity to excise it.
Researchers have discovered that neurons with double-stranded breaks (DSBs) in their DNA actively trigger an inflammatory response, which is mediated by the activation of the NFkappaB transcription factor. This process elicits an immune response from microglia, leading to synaptic loss and cognitive function impairment.
Scientists have made a groundbreaking discovery about the role of 'junk' DNA in neurological disorders such as Motor Neurone Disease and Alzheimer's. The research found that breaks in this type of DNA can lead to oxidative genomic damage, which can accelerate aging and disease progression.
Researchers uncovered crucial interactions between XPA and RPA proteins in NER, essential for repairing UV-damaged DNA. These findings hold promise for improving cancer therapy outcomes by targeting the NER pathway.
Researchers from Boston Children's Hospital found that aging heart muscle cells accumulate new genetic mutations over time, but lose the ability to repair them. This accumulation of mutations can push the heart past a tipping point into disease.
A recent study published in Aging-US reveals the crucial role of WRN in making choices between classical and alternative non-homologous end joining (NHEJ) DNA repair pathways. The research provides new insights into progeroid syndromes, such as Werner syndrome, and their connection to aging.
A new study from Karolinska Institutet shows how certain RNA molecules control the repair of damaged DNA in cancer cells. The researchers discovered two molecule types that interact to regulate an enzyme involved in DNA-repair mechanisms, leading to faulty DNA repair in cancer cells.
Scientists from CNIO and Massachusetts General Hospital have developed new approaches to visualize DNA repair by analyzing hundreds of proteins at once. They discovered nine new proteins involved in DNA repair and identified key players in the process, which could lead to improved cancer treatments.
A recent study published in PLOS ONE found that combining copper ions with a drug once used for treating alcoholism kills medulloblastoma cancer cells and prevents new ones from forming. The therapy also curtails the creation of cancer stem cells, which initiate tumor growth and recurrence.
Researchers at Princeton University developed a novel method called Repair-seq to understand genome editing tools, revealing complex mechanisms of DNA repair. This work improves the CRISPR gene-editing method by identifying new pathways and optimizing systems.
A study by the Center for Cell-Based Therapy in São Paulo, Brazil, has discovered a set of biomarkers that can be used to predict which patients with glioblastoma may have tumors resistant to radiation therapy. The genetic signature helps doctors choose the best treatment option for these patients.
Fels and Fox Chase researchers found specific TET2 and DNMT3A mutations in leukemia patients that affect DNA repair pathways. These mutations make leukemia cells sensitive to PARP inhibitors, a type of targeted therapy, while others are resistant. The study aims to develop personalized therapies for patients with these mutations.
The study describes the three-dimensional structure of the MUTYH protein and its interaction with PCNA, a key player in DNA replication. The researchers found that mutations in the MUTYH gene reduce its binding affinity to DNA and destabilize its structure, leading to decreased DNA repair activity.
Researchers identify a new class of mibefradil-based DNA repair inhibitors, which could be further advanced into pre-clinical testing and eventually clinical trials for glioblastoma radiosensitization. The compounds retain potency as DNA repair inhibitors while demonstrating reduced hERG and CYP450 enzyme inhibition.
Three UNIST graduate students, SangIn Kim, ByeongEun Lee, and YeonSong Choi, have been awarded the prestigious 2021 Asan Foundation Medical Bioscience Scholarship for their innovative work in DNA damage response, degenerative brain diseases, and disease genomics. The award provides financial assistance and recognizes their contribution...
Researchers at Mayo Clinic have developed LEAP, a proton therapy technique that targets cancer cells with defects in the ATM-BRCA1-BRCA2 DNA repair pathway, sparing surrounding normal tissues. The technique uses concentrated proton energy deposition to induce biologic responses in treatment-resistant cancers.
The article discusses the relationship between DNA repair pathways and cancer cells, highlighting five critical pathways and their impact on cancer evolution. The review suggests potential clinical interventions to address pathway damage, offering new insights into cancer treatment.
A new genome editing system has been developed to enhance the efficiency of an error-free DNA repair pathway, which could help improve agronomic traits in multiple crops. The system uses Cas9 and VirD2 to facilitate homology-directed repair, increasing the rate of precise genetic modifications.
Researchers created a mutated form of DNA repair protein RAD51 to study its critical functions at stalled replication forks. The study found that RAD51's strand exchange activity is not required for fork regression, but is crucial for restarting replication once the obstacle has been removed.
A new approach to gene editing has been developed by scientists at UMass Medical School, allowing for the correction of microduplications associated with 143 different diseases. The strategy uses CRISPR/Cas9 and harnesses the homology-directed repair pathway to remove duplicated sequences and restore functional genes.
Researchers found that tiny protein CYREN inhibits fast but error-prone NHEJ pathway and enables slower HR pathway, offering potential tool against cancer. CYREN's discovery clarifies longstanding mystery about DNA repair pathways.
Researchers developed a new gene-editing method called homology-independent targeted integration (HITI) that efficiently inserts DNA into genes in dividing and non-dividing cells of living rats. The technique uses the CRISPR-Cas9 tool to cut DNA at a specific location, followed by the NHEJ repair pathway for insertion.
Researchers discovered a novel mechanism by which adenovirus protein E4orf4 inhibits the DNA damage response, improving viral replication. This finding provides insight into the virus's ability to infect immunocompromised patients and may lead to new cancer therapies.
Researchers at Temple University Health System have discovered a small molecule inhibitor that selectively kills cancer cells with BRCA1 or BRCA2 gene mutations. The compound, 6-hydroxy-DL-dopa, works by blocking an alternative DNA repair pathway, providing a promising approach to precision medicine for various cancers.
Researchers from North Carolina State University have discovered how two important proofreader proteins, MutS and MutL, work together to signal the body's repair mechanism. The proteins use a unique communication system involving PCNA, which helps them identify and correct errors during DNA replication.
A new study by Lomonosov Moscow State University researchers clarifies the DNA alarm-system, which detects single-strand breaks and activates kinase ATM to signal repair. This system prevents cancer-causing mutations and cell death.
Researchers discovered a mechanism preventing mutation in genes involves long distance scanning of DNA by Mfd protein, detecting damage within active genes. This discovery sheds light on the complicated genome-wide patterns of mutation underlying species evolution and cell behavior changes.
Researchers studied how a protein complex called Mre11-Rad50 reshapes itself to take on different DNA-repair tasks, revealing insights into its dynamic structure and biological outcomes. The findings could guide the development of better cancer-fighting therapies and more effective gene therapies.
Scientists have discovered that DNA can act as a wire to detect genetic damage and identify people at risk for certain diseases. The discovery could lead to the development of medical diagnostic devices and biosensors that can pick up on changes in DNA that may lead to cancer and other diseases.
Researchers have elucidated the structure of a key protein involved in DNA double-strand break repair. The MRN complex plays a crucial role in cell survival and function, with mutations linked to distinct syndromes and predispositions to cancer, radiation sensitivity, and neurodegeneration.
A DNA repair pathway-focused score has been developed to predict chemotherapy response in ovarian cancer patients. The score is positively correlated with complete response rate, recurrence-free survival, and progression-free survival, and outperforms other clinical factors in predicting overall survival.
Scientists at Johns Hopkins have found that PARP inhibitors can block the ability of pre-leukemic cells to repair broken DNA, leading to their self-destruction. The treatment has shown promise in clinical trials for patients with aggressive myeloproliferative disorders.
UC Davis researchers have identified a new inducible pathway for repairing DNA damaged by oxygen radicals, which could lead to a better understanding of the causes of some cancers. The discovery involves an enzyme called NEIL1 that detects and repairs aberrant bases before changes in the genome become permanent.
Researchers develop method to target genes in Toxoplasma gondii, a parasite responsible for malaria and diarrhea. The breakthrough enables the creation of safe and effective genetically modified vaccines and drug therapies.
A study found that genetic variations in DNA repair genes can affect a person's risk of developing Hodgkin disease. Research suggests that differences in these genes could modify the risk of HD, with some individuals being up to four times more likely to develop the disease.
The study reveals that MDC1 plays a critical role in amplifying distress calls from injured DNA, triggering the repair process. This discovery provides insights into how cancer researchers can design new treatments to manage DNA damage and resist tumor formation.