Articles tagged with Mutant Cells
A new study co-led by TSRI scientists suggests that Ebola virus gained a genetic mutation, GP-A82V, which helps it better target human cells. This mutation emerged early in the epidemic and caused about 90% of infections during the recent outbreak.
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 researchers discovered that a specific mutation in the telomere protein TPP1 causes an incurable premature aging disease called dyskeratosis congenita. The mutation compromises telomerase function, leading to stem cell division slowdowns and tissue breakdown. This breakthrough provides a potential drug target for the disease.
Researchers have confirmed that mutation-caused dysfunction in a process cells use to transport molecules within the cell plays a previously suspected but underappreciated role in promoting Alzheimer's disease. The study found that treating mutated neurons with a beta-secretase inhibitor rescued endocytosis and transcytosis functions.
Researchers at the University of Illinois have observed transposon activity in real-time using fluorescent microscopy. The study reveals that jumping gene activation is dependent on environmental factors such as food availability.
Scientists at TSRI have discovered a mechanism that turns mutant cells into aggressive cancers. The research identifies the role of POT1 mutations and their impact on the cell's ability to repair DNA damage.
Scientists have confirmed that as people age, they accumulate gene mutations in their mitochondria, which can limit energy production and impair cellular function. Researchers recommend screening stem cells for mitochondrial DNA mutations to ensure their therapeutic value.
A recent study has found that induced pluripotent stem (iPS) cells derived from patient skin cells may contain faulty mitochondrial DNA mutations, which could undermine their therapeutic value. Screening and checking for mitochondrial DNA mutations is crucial to ensure the quality of iPS cell lines intended for therapeutic use.
Scientists have mapped thousands of genetic mutations in yeast to understand their impact on cell survival. The study found that different combinations of mutations can influence survival and revealed a new technique for predicting the shapes of molecules encoded in our genes.
Scientists at Rockefeller University have identified a new way for cells to die in the linker cell of Caenorhabditis elegans, resembling neuronal death in humans. The discovery suggests that this process might be involved in neurodegenerative disorders and could serve as a target for future drugs.
Researchers at CNIO have identified a protein, CDC25A, as a determinant of chemotherapy resistance in cancer cells. They used CRISPR genome editing technology to test various mutations and found that cells with this mutation were resistant to treatment.
Scientists at the Wellcome Trust Sanger Institute found that induced pluripotent stem (iPS) cells acquire fewer genetic mutations than lab-grown blood cells, reducing the risk of cancer. The study tracks the genetic history of iPS cells and provides insights into the mechanisms behind mutation rates.
Researchers at TSRI successfully sequenced individual neuron genomes and produced live mice carrying neuronal genomes in all of their cells. They found that each neuron contained an average of more than 100 mutations and accumulated more mutations in genes used frequently.
A team of Swiss and Russian scientists has deciphered how APOBEC takes advantage of a weakness in DNA replication to induce mutations, primarily affecting early-replicating genes. The study reveals that APOBEC targets single-stranded DNA regions during replication, which are more prone to mutations.
A new study proposes that genetic drift contributes to the development of leukemia in young children. The researchers used a computational model describing blood stem cell population dynamics and found that drift plays a significant role in early-life leukemia formation. In contrast, selection drives leukemia development in older adults.
Researchers suggest that a single mutation in protein interactions was crucial for the transition from single-celled to multi-cellular organisms. This discovery has implications for understanding disease states, such as cancer, where damaged cells can revert to a unicellular state.
Researchers found two clock-like mutational processes in human cells, correlated with age and potentially responsible for cancer and aging. The study analyzed 10,250 cancer genomes and identified 33 mutational signatures, revealing distinct mutation rates in different cell types.
A new study published in Science magazine reveals that vitamin C can selectively kill colorectal cancer cells with certain mutations, such as KRAS and BRAF. The research found that these mutated cells take up oxidized vitamin C through a specific receptor, leading to oxidative stress that inactivates an enzyme required for growth.
Scientists have discovered that brain cells contain significant numbers of somatic mutations, which contribute to human development and disease. The study provides a new perspective on the role of these post-conception mutations in shaping brain cell lineages and potentially driving neurodegenerative disorders.
A new study by HHMI scientists found that a single neuron in an adult human brain may have more than 1,000 genetic mutations not present in surrounding cells. These mutations mostly arise while genes are in active use after brain development is complete.
Researchers at Virginia Tech have refined a mathematical model that simulates genetic mutations and their impact on cell division. The model's accuracy has been improved through laboratory experiments and is expected to be useful in understanding how certain mutations thrive and reproduce, particularly in the context of cancer.
Researchers have developed a novel software that translates the effects of cancer mutations on protein function, revealing how disease mutations target and damage protein signaling networks within human cells. The discovery has significant implications for personalized precision cancer treatments.
Scientists developed an interactive analysis program called Gingko to study genetic anomalies and provide a simple way to visualize patterns in copy number mutations. This could help clinicians better target medications based on individual cell mutation profiles.
The study reveals that C9ORF72 mutations block the transfer of information between the nucleus and cytoplasm, leading to neuron deterioration. The research provides insight into developing targeted therapies for ALS and FTD.
The study reveals that the mutation disrupts normal cell function by interfering with RNA and protein movement into and out of the nucleus. This leads to neuronal deterioration and death in the brain and spinal cord, causing loss of voluntary muscle movement, paralysis, and respiratory failure.
Researchers have discovered a new mechanism by which bacteria can develop resistance to antibiotics, called retromutagenesis. This process involves mutations occurring in RNA first, allowing cells to grow and replicate before subsequent DNA mutations can take effect.
A new model suggests that evolutionary pressures from healthy tissue keep cells with cancerous mutations in check. The study proposes that the ecosystem of a healthy tissue landscape allows healthy cells to outcompete those with cancerous mutations, but when this balance changes due to aging or stressors, cancer cells can thrive.
Researchers developed a screening test to measure mutant huntingtin protein seeding in cerebrospinal fluid, distinguishing symptomatic Huntington's patients from gene carriers. This assay may accelerate the development of new drugs to treat this incurable disease by blocking cell-to-cell seeding.
A new study finds that measles virus has rigid surface proteins that can't tolerate mutations, making it less prone to evolution than the flu virus. This difference in protein stability may explain why measles only requires a two-dose vaccine during childhood for lifelong immunity.
Researchers discovered a key gene that shields us from fungal and bacterial infections, and found it affects two crucial cell types involved in our immune response. STAT3 helps regulate the development and function of natural killer T and mucosal-associated invariant T cells, which play a vital role in fighting off pathogens.
Researchers at Salk Institute have developed a new method to convert cells from x-linked SCID patients into stem cell-like state, fix the genetic mutation and prompt corrected cells to successfully generate NK cells in the laboratory. This technique could lead to a more effective and less invasive treatment for this devastating disease.
Researchers estimate that up to 20% of people aged 50-60 and more than 70% of people over 90 have blood cells with the same gene changes as found in leukemia. Genetic mutations associated with leukaemia become inevitable with age, increasing dramatically with age.
A new technique allows scientists to trace and spatially map 'mosaic' mutations in the brain, providing a significant advance for genetics research. This capability enables the study of both normal brains and brain disorders such as epilepsy and autism, offering new avenues for investigation.
Researchers uncover that C9orf72 gene mutation generates toxic PR protein causing brain damage in ALS, leading to motor neuron death. This discovery may lead to new treatments by preventing or breaking down PR aggregates.
Researchers found malignant mesothelioma tumors to be polyclonal, resulting from the growth of multiple mutant cells. This challenges the long-held belief that cancers are caused by a single cell mutation.
Researchers discovered a mutation in adult fruit flies that prevents testicular cells from transforming into ovaries, maintaining sex identity. The study's findings have implications for understanding cell fate conversions and may lead to new therapeutic approaches.
Phase II data showed dabrafenib has significant anti-tumour activity in patients with advanced BRAF V600E mutant non-small cell lung cancer. HER2 inhibition also shows promise in HER2-positive non-small cell lung cancer, with a 21% overall response rate in patients treated with neratinib and temsirolimus.
Researchers used induced pluripotent stem cells to compare heart muscle cell survival decisions in people with and without a genetic mutation. They found that the mutation affects heart health by controlling cell survival during stress, and identified a protein involved in programmed cell death.
Researchers have found that using gene-editing techniques on stem cells does not increase the overall occurrence of mutations, easing previous safety concerns. The study's results were published in the journal Cell Stem Cell and provide new hope for the development of therapies for genetic diseases.
By analyzing somatic mutations in healthy cells, researchers can reconstruct a cell's development from the early embryo to adulthood. This approach provides insight into normal cell development and could help understand how it differs from cancerous cells.
A recent study has identified five essential mutations allowing the H5N1 bird flu virus to spread through the air between ferrets. These findings could provide crucial insights for future surveillance and early warning systems, potentially preventing future pandemics.
A recent study by researchers at Penn Medicine has discovered the essential role of tumor suppressor gene FLCN in regulating lung function in patients with Birt-Hogg-Dube (BHD) syndrome. The absence or mutation of FLCN leads to deteriorated lung integrity and impaired lung function, as reported in their findings in Cell Reports.
A new study reveals that defective ribosomes are the root cause of human diseases, starting with anemia and bone marrow failure early in life. As quality control systems fail, more ribosomes become available, leading to changes in gene expression patterns that can result in cancer.
Researchers found that the initial stage of autophagy is not directly related to the composition of the Beclin-1 complex. Instead, other mechanisms are likely involved in inducing autophagy. This study highlights the complexity of autophagy regulation and challenges current understanding of its role in neurodegenerative diseases.
Researchers found that the C9orf72 mutation alters DNA shape, leading to cell death and abnormal protein processing. The mutation also affects nucleolin, a key protein involved in stress response, causing cells to become stressed and die.
Scientists have created a new statistical method to analyze individual cells, allowing for more accurate detection of cell properties. By combining data from multiple cells, researchers can reduce errors and overcome statistical noise, leading to better understanding of cellular behavior and development.
Scientists have discovered molecules that may block the accumulation of a toxic eye protein leading to early onset glaucoma. The researchers identified two compounds with potential for future drug development to treat this condition, which affects several million people from childhood to age 35.
Researchers found that ALS protein Fus promotes the translation of RNAs in cells with cytoplasmic granules similar to those in ALS patients. This suggests a new mechanism contributing to disease symptoms, where misdirection of RNA translation rather than silencing drives pathology.
Researchers have developed a new therapy that targets the C9ORF72 gene mutation causing dementia and ALS. The stem cell-based approach manipulates brain cells in test tube studies, discovering compounds that counteract the genetic glitch.
A study at the Weizmann Institute suggests that in a quarter of all leukemias, cancer cells use a balance between a mutated gene and its normal counterpart to keep going. The healthy RUNX1 gene plays a crucial role in blood cell development and maintenance.
Researchers have discovered a network of genes in stem cells that foster cooperation, which is essential for the development and function of multicellular organisms. The study suggests that understanding this genetic mechanism could lead to new ways to address diseases such as cancer and immune system dysfunction.
Scientists develop a new approach to eliminate mutated DNA in mitochondria using TALEN technology inspired by plant-infecting bacteria. The method shows promise for treating mitochondrial diseases, including Leber hereditary optic neuropathy, and could lead to effective treatments for various eye diseases.
Researchers discovered a mutated protein that selectively enhances cancer cells while sparing healthy ones. The findings suggest a potent new therapeutic target for certain types of leukemia.
Researchers have found that common mutant forms of the JC polyomavirus are not infectious, but may still contribute to disease. The mutants appear to be up to no good by only being found in immunocompromised patients and possibly helping the main virus evade the immune system.
Researchers at Sanford-Burnham Medical Research Institute discovered that three children with Congenital Disorders of Glycosylation had mutation-only in some cell types, raising questions about inheritance and genomic sequencing. The study highlights the importance of using multiple diagnostic tests to accurately diagnose rare diseases.
Researchers at Johns Hopkins Medicine found how a gout-linked genetic mutation causes disease by breaking a cellular pump that clears uric acid waste. They identified a compound that partially repairs the pump in laboratory tests.
Researchers have discovered that broadly neutralizing antibodies (bNAbs) can handle HIV's high mutation rate, offering a promising strategy for vaccine development. The study found that mutations in framework regions strengthened the antibodies' antiviral activity while conserving key structural features.
A team of researchers has discovered a significant mutation in a LINC family protein that could lead to new treatments for hearing disorders. The mutation causes chaos in the cell's anatomy, leading to devastating effects on cells responsible for hearing.
Researchers identify normalizing p62 levels in immune system cells as a strategy to clear an infection that is deadly to patients with cystic fibrosis. This approach enables the natural cellular process of autophagy, which helps digest pathogens and clear them away, thereby controlling inflammation and saving patients from death.
A recent study from Baylor College of Medicine describes an elaborate gene network that functions in causing mutations during DNA repair in stressed cells. The network, composed of 93 genes, regulates the production of mutations in response to environmental challenges such as starvation or antibiotics.