Articles tagged with Mutant Cells
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A new simulation model describes various modes of cancer evolution in a unified manner, shedding light on therapeutic resistance and novel strategies. The study found that linear evolution occurs with strong driver mutations, while intratumor heterogeneity is shaped by natural selection or neutral evolution.
Researchers at Cincinnati Children's Hospital Medical Center create a new platform to study the single-cell genomics of various diseases, potentially making genetic-based diagnoses more precise and effective. The study focuses on linking gene mutations to disease-causing processes in blood diseases like severe congenital neutropenia.
A team of researchers led by University of Delaware Professor Velia M. Fowler has made a groundbreaking discovery about MYH9-related disorders, a condition affecting 1 in 25,000 people. The study found that mutations in the MYH9 gene disrupt platelet formation and movement, leading to unstable clots and various health issues.
Scientists have found that 'silent' genetic variations in DNA sequences can significantly impact protein folding, impairing cell function. The study, conducted by the University of Notre Dame, used a bacterium to test this hypothesis, finding that synonymous mutations can alter protein synthesis rates.
Researchers found that mutations in gene ydcI cause increased numbers of persisters, a type of bacteria resistant to antibiotics. Persisters have memory loss, leading to abnormal growth and making them difficult to treat.
Researchers have developed a new technique to detect point mutations relevant to human health, providing accurate early diagnosis and guiding therapy. The method, called SNIPRs, can be applied in living cells and offers a rapid, highly accurate, and inexpensive means of identifying mutations.
A team of researchers at the Garvan Institute of Medical Research has identified individual cells that cause autoimmune disease from patient samples. They discovered how these cells 'go rogue' by evading checkpoints and accumulating genetic mutations that drive disease progression.
A new paper explores how bodies evolve to prevent cancer by making growth factors costly to use and limiting cell proliferation. Individual cancer cells are kept in check when there's a high energetic cost for creating growth factors that signal cell growth.
New study finds low doses of ionizing radiation used in medical imaging create breaks that allow extra bits of DNA to integrate into the chromosome, potentially leading to mutations. The researchers stress that translating these findings to animal models is necessary to determine full effects and impact on patient health.
New research suggests lactate is a catalyst that triggers cancer forming process in mutated cells. The study's findings open a new door to better understand cancer at the metabolic level and could lead to targeted therapies.
Researchers have made a breakthrough in understanding cancer prediction by developing a new method to evaluate cell dynamics and tumor initiation. Their calculations reveal that fixation times are a more important metric than lifetime risks, and that some mutated cells may fix tumors faster than expected.
Researchers identified Annexin A6 as a key factor in cholesterol regulation and potential therapeutic target for diseases caused by lipid accumulation. The study shows that silencing AnxA6 can redirect cholesterol to other cell compartments, potentially treating conditions like Niemann-Pick type C1 and various cancers.
A new bioinformatics tool, MHcut, reveals that microhomology-mediated end joining is more common in humans than previously thought. Using this tool and commercial genome-editing technology, researchers created precise gene mutations to model diseases, providing insights into rare and orphan diseases.
Researchers used in vivo imaging to observe how cells move and generate forces in living tissues, revealing new clues on why MYH9 gene mutations lead to various diseases. The study demonstrates that altered myosin activity results in defects in epithelial morphogenesis due to slower cell movements.
Researchers have identified a genetic mutation in the SFTPA1 gene that causes idiopathic pulmonary fibrosis (IPF), a progressive lung disease characterized by scar tissue buildup. Inhibiting necroptosis, a cell death pathway, could be a new therapeutic approach to treating IPF.
Researchers discovered that long-lived fungi accumulate surprisingly few mutations over time, indicating a well-developed protection mechanism. The study uses fairy rings of Marasmius oreades to examine the speed and pattern of mutations, providing new insights into cell processes and longevity.
A new study published in Nature reveals the full spectrum of cells involved in congenital heart defect formation, identifying key cell types and their functions. The research uses single-cell RNA sequencing to uncover the molecular drivers of different cell types, shedding light on genetic mutations and disease mechanisms.
Researchers at the Wellcome Sanger Institute found that low doses of radiation increase p53 mutations, giving cancer-capable cells a competitive advantage. However, antioxidants can boost healthy cells to outcompete mutant cells.
Researchers at Stanford University School of Medicine identified a genetic mutation linked to dilated cardiomyopathy, a disease characterized by an enlarged heart's main pumping chamber. They found that treating patient-derived heart cells with existing drug inhibitors corrected the mutation's effects.
A new study finds that cancer incidence increases uniformly with age, contradicting the traditional model of oncogenesis. The research suggests that selection pressure acting on healthy cells and cancer cells determines who gets cancer, with a shift in favor of cancer-causing mutations in older age.
A comprehensive RNA sequence analysis reveals that normal cell populations contain lineages of mutational mosaics, with sun-exposed skin and throat tissues developing more mutations. The study's findings suggest a link between age, cell proliferation rate, and environmental exposure to cancer risk.
A new approach detects mutations across many different types of normal cells by analyzing RNA sequencing data from normal tissues. The study found that 95% of individuals had at least one tissue with mutations, with higher rates in lung, esophagus, and sun-exposed skin.
A new study reveals that actin, a protein responsible for cell movement, also drives the ability of cancer cells to grow when under stress. Enlarged actin sheets called lamellipodia sequester tumor suppressor molecules, allowing cancer cells to resist chemotherapy and grow more aggressively.
Researchers discovered that transcription factors ANAC044 and ANAC085 control plant cell cycle arrest in response to DNA damage and abiotic stress. These proteins act as a bridge between SOG1 and Rep-MYB, preventing cell proliferation under hostile conditions.
A team of researchers has identified a genetic pathway that causes some individuals to develop an abnormal heart rhythm after experiencing a heart attack. They have also discovered a drug candidate that can block this pathway.
Researchers propose a new perspective on cancer origins, highlighting the importance of mutation sequence and cell type in tumor growth and response to therapy. This approach may lead to new avenues for cancer prevention and treatment.
Researchers used single-cell RNA sequencing to study gene expression in individual cells and identify unique therapeutic targets for cancers that form in specific cell types. The study found that mutations in certain genes can make cells vulnerable to apoptosis, providing a potential way to prevent or treat cancer.
A machine-learning algorithm, inDelphi, predicts the precise correction of broken genes by analyzing data from CRISPR-induced breaks. Researchers successfully corrected nearly 200 disease-associated genetic variants, restoring gene function to healthy states.
Researchers found that a genetic defect tied to ALS and other neurodegenerative diseases leads to increased lipid production in starved cells. The mutation alters the regulation of lipid metabolism pathways, increasing levels of enzymes like NOX2, which can damage cells.
Researchers discovered that cancer-associated genetic mutations are prevalent in healthy esophageal epithelium tissue, accumulating with age. By middle age, over half of the tissue contained mutant clones, suggesting a potential origin for esophageal cancers.
Researchers have developed a new approach to understand cancer's complex causes, enabling the analysis of multiple gene mutations simultaneously. This will accelerate the development of new treatments and provide insights into strategies for stopping cancer formation and spread.
Scientists discover that healthy oesophagus tissue contains hundreds to thousands of mutations per cell by middle age, with only a dozen genes driving competition. The study reevaluates the role of some cancer genes in light of normal tissue sequencing, raising new questions about ageing and disease progression.
Researchers developed a microtissue model of the heart to study how environmental stress affects normal and abnormal heart tissue. The study found that mutant cells contracted abnormally and arrhythmically under stress, similar to HCM patients.
Researchers develop a method to continuously record cells' development using genetic barcodes, allowing them to trace the full developmental lineage of every mature cell. This breakthrough resolves longstanding questions about brain patterning and promises to exponentially increase understanding of cellular growth and disease emergence.
Researchers reveal how oncogenic mutant cells selectively occupy space in tissues without cell division. They found that after the death of normal cells, oncogenic mutant cells expanded through rearrangement of the honeycomb packing pattern.
Researchers developed a computer model that forecasts tumour changes, allowing for early disease course prediction and personalized treatment. The study reveals driver mutations can accelerate tumour growth by up to 30%.
Advances in genetic testing have improved insights for parents of children with epileptic encephalopathy (EE), a rare and serious form of epilepsy. The study found that 10% of parents have mosaicism, which may also apply to other disorders like autism and intellectual disability.
Researchers discovered that larger, more visible SOD1 protein aggregates are protective rather than harmful to neurons. The study suggests that these fibrils could be a solution to reduce toxicity in SOD1-ALS, and finding drugs to promote their formation may help mitigate the disease.
Scientists have developed a new CRISPR method to analyze the effects of thousands of gene edits in parallel, improving their ability to identify harmful genetic changes. This technique enables researchers to rapidly distinguish between damaging and harmless edits, potentially leading to breakthroughs in disease diagnosis and treatment.
Researchers at Johns Hopkins Medicine have uncovered a link between a genetic mutation in the GBA1 gene and the formation of fatty plaques in the brain that contribute to Parkinson's disease. The study found that changes in the mixture of fatty molecules cause protein pieces to stick together, forming 'dead zones' in the brain.
Researchers at Karolinska Institutet discover high number of mutations in muscle stem cells impairing cell regeneration, which may result in new medication for building stronger muscles. The study found that physical exercise could clear out cells with many mutations.
Researchers develop CRISPR-Cas9 gene editing therapy to prevent hearing loss in a mouse model of human genetic progressive deafness. The therapy delivers the protein complex directly into sound-sensing cells, disrupting the mutation that causes cell death and preserving some hearing.
Scientists at Salk Institute develop novel approach to discover critical contacts on proteins, uncovering new functions for well-studied proteins. The technique has significant implications for therapeutic drug development, which relies heavily on physical interaction with cellular targets.
Researchers have discovered a cocktail of drugs that effectively eliminate acute myeloid leukemia (AML) by targeting key pathways. By simultaneously blocking two important pathways, the team was able to achieve complete elimination of AML in most cases tested.
Researchers have made a breakthrough in treating alpha-1 antitrypsin deficiency by using a new gene editing technique. The approach combines RNA interference and gene augmentation to repopulate diseased livers with healthy cells, preventing damage and promoting regeneration.
Researchers found that new mutations in iPS cells are concentrated in non-transcriptional regions of the genome, which are sensitive to oxidative stress. This suggests that these mutations may not lead to cancer-related adverse effects.
Scientists have developed a way to generate and correct specific lung cells using pluripotent stem cells, which could lead to new therapies for conditions like neonatal respiratory distress and COPD. The corrected cells were able to produce essential surfactant, previously an elusive milestone.
Researchers successfully corrected a heart condition-causing mutation in human embryos, paving the way for potential treatments and prevention of inherited diseases. The technique uses CRISPR-Cas9 to target specific genetic mutations, offering hope for improving IVF outcomes and curing certain diseases.
A new evolutionary theory of cancer suggests that cells with dangerous mutations exist all the time but are commonly outcompeted by healthy cells in healthy tissues. However, when the tissue microenvironment is damaged, these pre-cancer cells can thrive and establish themselves in the body.
Finnish researchers discovered gene mutations in white blood cells of patients with rheumatoid arthritis, which accumulate similarly to cancer-causing mutations. The mutations were found only in mature T cells and had a permanent impact on the disease.
Researchers found that human pluripotent stem cells can acquire mutations in the TP53 gene, a tumor suppressor responsible for controlling cell growth and division, highlighting the need for genetic screening methods to exclude mutated cells from scientific experiments and clinical therapies.
Researchers at the University of Helsinki have discovered that premature cell differentiation caused by a STAT3 gene mutation can lead to underdeveloped pancreas and early onset of neonatal diabetes. The study used induced pluripotent stem cells to examine the impact of the mutation on pancreatic development.
A new study sheds light on the dark side of tumor suppressor gene p53, revealing that regulating genes Mdm2 and Mdm4 keep mutated p53 in check. The study shows that mutating these proteins can lead to an elevation of mutant p53, driving cancer growth.
Researchers at NHGRI found that iPSCs have the same mutation rate as subcloned cells, providing evidence of their stability and safety. This breakthrough enables further research and potential therapy development using patient-specific iPSCs.
Researchers have found that activating the protein Nrf2 can restore normal levels of disease-causing proteins in cells, preventing cell death. In models of Parkinson's and Huntington's diseases, Nrf2 was shown to protect cells against the disease better than any other treatment.
Researchers found that KRAS mutant cancer cells form more stress granules in response to chemotherapy, making them harder to kill. A new compound target, 15-d-PGJ2, may help improve treatment outcomes by blocking this coping mechanism.
Researchers found genetic mutations increased with donor age, particularly in late 80s and early 90s donors, which could impact iPSC therapies. Screening is crucial to filter out defects and ensure safe treatment.
Researchers have mapped the developmental stages of mouse heart cells, revealing previously unknown cell types and insights into congenital heart defects. The study's findings provide a temporal and spatial atlas of heart cell populations, paving the way for understanding human cardiovascular system development.
Researchers found that smoking one packet of cigarettes a day accumulates an average of 150 extra mutations in every lung cell, leading to increased cancer risk. The study also identified molecular fingerprints of DNA damage in smokers' DNA, revealing the complex mechanisms behind tobacco-related cancers.
A team of scientists discovered a comprehensive set of suppressive mutations in yeast cells, which could help explain how some people remain healthy despite carrying catastrophic mutations. The findings provide new insights into the complex relationship between genetic suppression and disease-causing mutations.