Articles tagged with Cancer Cells
A novel HIPK2 isoform is identified that promotes YAP/TEAD transcriptional activity in non-small cell lung cancer cells. The study suggests that this isoform may play an oncogenic role in NSCLC and could be a potential therapeutic target.
The ADAR1p110 isoform regulates genome stability at chromosome ends, preventing R-loop accumulation and preserving telomere stability. In cancer cells, depletion of ADAR1p110 leads to extensive telomeric DNA damage and arrested proliferation.
Researchers at Harvard University have designed a new highly-selective tool to study proteins that are difficult to target with drugs, known as 'undruggable' proteins. The tool uses a nanobody to add or remove specific sugars from proteins, providing a detailed understanding of their function.
Researchers used an experimental safety switch to curb treatment side effects in a patient with refractory acute B-cell leukemia, achieving a significant reduction in toxicities. The study demonstrates potential for expanded use of CAR-T immunotherapy paired with the safety switch.
Researchers develop targeted immunotherapy approach that specifically kills cancer cells by targeting mutant protein fragments presented on the cell surface. The therapy uses bispecific antibodies to recognize and destroy cancer cells, bypassing conventional antibody limitations.
Scientists at Far Eastern Federal University have developed a compound that kills prostate cancer cells while also activating an enzyme protecting them. The compound, 3,10-dibromofascaplysin, works well in combination with approved anticancer drugs and is being studied for its potential to reduce side effects.
Researchers develop bispecific T-cell engaging antibodies that target cancer cells and stimulate the immune system without removing T-cells. This approach could make personalized treatments more broadly accessible and potentially transform cancer into a chronic disease.
Researchers discovered artificial microswimmers slow down and accumulate in low-fuel regions where their speed is minimized. This finding suggests a new strategy to improve targeted cancer therapy by delivering chemotherapy drugs to the most problematic cells.
Researchers have discovered a gene called ENDU-2 that can trigger tumor formation from a distance while also protecting cells under stress. In the nematode worm C. elegans, ENDU-2 helps protect germline immortality, suggesting its role in cancer development and cell survival.
Researchers develop a new protein, 161519 TriKE, to target cold tumors and enhance the immune response. The study found that 161519 TriKE successfully reduced tumor growth and increased overall survival in tumor-bearing mice.
Researchers have successfully 'caught' colibactin, a genotoxin from E. coli, inducing genetic changes characteristic of colorectal cancer cells. This breakthrough enables the observation of transformation in vitro using human colon organoids.
Researchers studied cell interactions in a microscopic 'cell collider' and found that normal cells repel each other's protrusions, while cancer cells try to squeeze past each other. The study suggests new approaches for understanding cancer cell behavior and identifying molecular bases for these differences.
A study published in Oncotarget found that hemoglobin-based oxygen carriers increase chemotherapy effectiveness in non-small cell lung cancer. PolyHb administration attenuates tumor growth without alleviating hypoxia, suggesting a potential strategy to enhance cisplatin sensitivity.
A study published in Cell Death & Disease found that inhibiting the EZH2 protein can reduce cancer cell growth in multiple myeloma. The researchers discovered that certain metabolic pathways are altered in cells sensitive to EZH2 inhibition, providing potential markers for treatment response.
Researchers at Lund University discovered how E. coli bacteria target and degrade the MYC oncogene, a well-known contributor to many forms of cancer. This discovery has shown potent effects on tumor growth and increased survival in two different cancer models.
Research on T cells reveals that prolonged exposure to antigens can lead to exhaustion, reducing their ability to contribute to immune responses. A new model study identifies dynamic adjustments in T helper cells' states of exhaustion and suggests potential therapeutic targets.
Researchers developed a new strategy to destroy cancer cells using magnetic nanoparticles and constant magnetic fields. The combined effect of nanoparticles and magnetic fields reduced the viability of leukemia cells while sparing healthy cells, suggesting a selective therapeutic effect.
Researchers at University of Helsinki discovered a molecular mechanism that promotes cell migration by recycling actin filaments. Twinfilin efficiently removes Capping Protein from filament plus-ends, leading to depolymerization and slower cell migration in its absence.
The study shows that the BAF complex plays a crucial role in controlling DNA accessibility and that its inhibition leads to rapid changes in chromatin structure. This has significant implications for understanding cancer development and identifying potential therapeutic targets.
A new synthetic gene circuit process allows for more effective disease treatment by preventing cancer cells from metastasizing and making them receptive to treatment. The technology, developed at Arizona State University, has broad implications for improving the effectiveness of various disease therapies.
Researchers at Technion-Israel Institute of Technology have discovered a new pathway that targets cancer cells specifically, minimizing damage to healthy cells. The folate cycle is essential for DNA and RNA production, and the team found that tumor cells relying on the cytosolic pathway are more susceptible to targeted treatments.
The study investigates the role of cell cycle progression on analyzing telomerase activity in cancer cells based on an AIEgen-based fluorescence detecting system. The results show that cancer cells exhibit increased fluorescence intensity during different stages of the cell cycle, while normal cells do not.
Researchers at the Max Delbrück Center used advanced microscopy to determine that CXCR4 receptor on cancer cells appears in both transient pairs and alone, depending on receptor density. This knowledge may lead to more effective cancer drugs with fewer side effects.
Researchers at the University of Seville have solved a long-standing enigma in basic biology by discovering how lipids distribute proteins within cells. Using a new microscopy technology, they found that membrane lipids select and direct specific proteins to correct exit doors.
Researchers have identified a key function of AIM2, a molecule that plays a vital role in regulating the adaptive immune system. The study reveals that AIM2 is expressed at higher levels in regulatory T cells, which prevent overzealous immune responses and mitigate autoimmune diseases.
Researchers develop innovative approach to treating bone tumors by starving cancer cells of their energy source, potentially replacing toxic chemo with a less harmful treatment. The two-drug combination showed promise in mice studies, outperforming a commonly used chemotherapy drug without severe side effects.
Researchers used XSEDE Stampede2 supercomputer to simulate polarized elongation of actin filaments, shedding light on their polymerization kinetics. The study's findings have potential applications in cancer treatment and development of self-healing materials.
A new method has been developed to identify peptides that inhibit histone deacetylases (HDACs), enzymes that play a role in cancer development and treatment. The researchers hope to use this method to develop more specific HDAC inhibitors with fewer side effects, leading to improved cancer therapy.
Researchers at Northwestern University have developed a novel therapy that uses synthetic nanoparticles to trigger the destruction of lymphoma cells by depriving them of cholesterol. This approach has potential for targeting other cancers with an appetite for cholesterol, such as kidney and ovarian cancer.
Researchers at Toyohashi University of Technology developed a low-cost method for intracellular delivery using titanium-oxide nanotubes and nanosecond pulse lasers. The study successfully delivered propidium iodide and fluorescent dextran into HeLa cells with high efficiency and cell viability.
Scientists have discovered a previously unknown enzymatic function of the Epstein-Barr Virus (EBV) protein EBNA1, which could lead to new approaches for treating EBV-associated cancers. The study sheds light on how this protein helps replicate and maintain the viral genome in infected cells.
Using CRISPR, scientists have created 'scratchpad' cells that can be tracked in real-time as they proliferate and spread. This method reveals differences in tumor biology and identifies genes associated with metastasis.
Researchers at Sloan Kettering Institute found a new link between Warburg metabolism and PI3 kinase activity, challenging the long-held view that metabolism is secondary to cell signaling. The study suggests targeting metabolism could be an effective way to curb cancer growth.
A new method traces real-time cancer progression across thousands of cells, identifying rare events and distinct gene expression profiles associated with metastatic phenotypes. The approach could inform aspects of cellular cancer biology, including genetic mutations, microenvironment adaptation and resistance to therapeutic agents.
Researchers at Moffitt Cancer Center discovered that cancer cells can fuse and recombine their genetic material, leading to increased diversity and adaptability. This mechanism, similar to parasexual recombination in pathogenic microbes, enables cancer cells to rapidly evolve and acquire resistance to treatments.
A new method, D2O-CANST-R, allows for rapid and precise tracking of metabolic changes in cancer cells at the single-cell and single-organelle level. This approach has the potential to reveal the metabolism in a cancer cell with very fine details and distinguish between effective and ineffective drugs.
Cell velocity depends on surface stickiness, and researchers have figured out the precise mechanics. A mathematical model captures forces involved in cell movement, matching experimental results for various cell types. The findings could provide new targets to interrupt tumor metastasis.
Researchers from UC3M and UCM developed a mathematical model to understand how cancer cells invade healthy tissue, using topological data analysis techniques. The model simulates the collective movement of cells in tissues and can be used to track the progression of tumor growth.
Researchers created nanodiamond sensors that can act as both heat sources and thermometers, allowing for the measurement of thermal conductivity inside living cells. This breakthrough may lead to new diagnostics tools and cancer therapies, as well as a better understanding of metabolic disorders such as obesity.
Researchers at UNH discovered a new inhibitor drug combination that effectively reduces growth and kills WM cancer cells, offering more treatment options. Adding venetoclax or panabinostat to BET inhibitors shows improved efficacy in treating Waldenström macroglobulinemia.
Researchers at Moffitt Cancer Center have identified a novel biochemical pathway that protects cells from ferroptosis, a type of cell death caused by oxidation imbalance. The discovery involves the activation of the protein GCLC, which leads to the production of gamma-glutamyl-peptides that shield cells against ferroptosis.
Researchers discovered that ovarian cancer cells undergo structural changes in their mitochondria to survive and proliferate in the peritoneal cavity. This adaptation enables aggressive cancerous cells to grow and spread, making it harder to detect and treat. Understanding these cellular adaptations could lead to new targeted therapies.
Scientists have created glowing probes to visualize four-stranded DNA in living cells, revealing its interaction with molecules and shedding light on its role in cancer and other diseases. The discovery opens up new avenues for research and potential drug development.
This issue of APSB features studies on the anticancer effects of berberine, baicalein's potent antivirus ability against HSV-1, and a new class of PDE10A inhibitors for treating PAH. Additionally, several articles explore innovative drug delivery systems and novel targets for cancer therapy.
Scientists have created a new method for combating non-Hodgkin's lymphomas by equipping immune cells with an antenna that targets the CXCR5 receptor on cancer cells. In laboratory experiments and mouse models, this approach showed promising results in fighting follicular lymphoma and chronic lymphocytic leukemia.
Scientists at the University of Southampton have discovered that modifying antibodies to target OX40 can enhance immune responses against cancer cells. By adjusting the antibody's isotype, researchers found that one type can delete suppressive Treg cells and another can stimulate killer T-cells, leading to improved anti-tumor effects.
Researchers at UCSF have discovered a new method to control immune responses using CD47-expressing hypoimmune stem cells. These cells can silence natural killer cells via the SIRPα checkpoint, paving the way for novel cell therapies and tissue implants that can evade immune rejection.
Researchers have found that cancer cells can enter a slow-dividing state to survive chemotherapy, similar to an embryonic survival program in mammals. Targeting these sleeping cells with novel therapies may prevent cancer regrowth and overcome drug resistance.
A biologist has created software tools to model cancer pathways and predict the efficacy of cancer drugs. The project aims to develop targeted treatments that target specific signaling networks in cancer cells, reducing harm to normal cells.
Researchers at Kyoto University's iCeMS have discovered how a transporter protein twists and squeezes compounds out of cells, including chemotherapy drugs from some cancer cells. This mechanism, driven by ATP energy, facilitates the export of toxic compounds and confers drug resistance.
Researchers found that chromothripsis breaks up chromosomes, leading to the formation of rearranged genomes and extra-chromosomal DNA that promotes cancer cell growth and drug resistance. This phenomenon enables cancer cells to evade treatment and become more aggressive.
Researchers discovered SETD2 modifies actin cytoskeleton, regulating cell migration and autophagy. Defects in SETD2 lead to impaired delivery of chromosomes and separation of daughter cells during cell division.
Researchers found that reduced amounts of p120ctn contribute to resistance in cancers with high EGFR levels, leading to poorer treatment outcomes. Testing for p120ctn levels may help clinicians identify patients at risk for therapy resistance or relapse.
Researchers have developed nanoparticles that can breach cell barriers and kill tumor cells, reducing tumor sizes by 40-70% in mice. The highly selective toxicity of the particles offers new hope for treating aggressive cancers.
Studies found that DNA leakage from cell nuclei triggers an immune response in cancer cells, making them more susceptible to immunotherapy. Delivering radiation before immunotherapy may be an effective way to fight challenging-to-treat cancers.
A team of researchers has identified a protein called RFWD3 that plays a critical role in recruiting DNA repair and signaling factors. The discovery could lead to new methods to inhibit these repair processes, making chemotherapy more efficient and reducing side effects.
Researchers developed inhibitors targeting mitochondrial DNA, affecting only rapidly dividing cells like cancer cells. Treatment stopped cell proliferation and reduced tumour growth without harming healthy cells.
Researchers at Scripps Research Institute have successfully modified natural killer cells to selectively target and destroy lymphoma cells, a promising breakthrough in cancer treatment. The innovative approach uses glycans, sugar-like molecules that play crucial roles in disease, to steer the cells to malignant B-cells.
Tumor cells produce excess complement protein iC3b to mask abnormal proteins, evading immune cell attack. The immune system relies on a flexible receptor CR3 to distinguish between 'I belong' and 'I don't belong' tags.
A recent study published in Oncogenesis suggests that a compound derived from the thunder god vine can attack 'super-enhancers' in the DNA of cancer cells, as well as the stroma surrounding the tumor. This disruption leads to accelerated cancer cell death and improved clinical outcomes for pancreatic cancer patients.