Articles tagged with Cancer Cells
A Mayo Clinic study has found that exhaustion affects immune cells fighting cancer, rendering them less effective. The research suggests a new approach to lymphoma and other cancers by dampening cell-signaling molecules like IL-12.
Two UC Davis faculty members, Frederic Chedin and Noriko Satake, received Individual Biomedical Research Awards to explore novel approaches to understanding autoimmune diseases. Paula Goines, a postdoctoral researcher, will also receive funding for her work on autism research using nerve cells grown from adult stem cells.
The University of California, Santa Cruz, has established the Cancer Genomics Hub to manage and analyze large-scale cancer genomic data. This hub will support research programs like The Cancer Genome Atlas and enable personalized cancer care by connecting specific genomic changes with clinical outcomes.
Researchers have made a groundbreaking observation of cellular architecture using high-powered microscopes, revealing the structure of microtubules during gamete formation. The findings could impact the treatment of diseases caused by misregulation of microtubule structures, including Down syndrome and cancer.
Researchers have created a new instrument that rapidly analyzes the physical properties of cells to identify cancer and other cell states. The deformability cytometer measures cells' responses to fluid flow, providing valuable information about cell health.
Researchers have identified a second form of the MCL1 protein, which works in a different location and performs a different function. The newly discovered version is shorter and located inside mitochondria, where it promotes mitochondrial energy production and may aid in cancer treatment.
Researchers have found that adding boron-nitride nanotubes to cancer cells can increase the effectiveness of a minimally invasive treatment for soft tissue tumors. The treatment, known as Irreversible Electroporation, has been shown to kill twice as many cancer cells when BNNTs are present on the cell surface.
Researchers at Simon Fraser University found that cholesterol-binding proteins called ORPs can control cell growth, potentially slowing down cancer cells. Genetic changes blocked the ability of these proteins to bind cholesterol, but altered ORPs actually stimulated cell growth by activating regulator proteins.
Researchers at Huntsman Cancer Institute have discovered that normal epithelium tissue ejects living cells to maintain a steady population and ease overcrowding. This mechanism is crucial in preventing cancer, as it allows cells to turnover and prevents cell pile-ups, which are common in cancerous tissues.
Researchers create iPhage particles that penetrate cells using penetratin, targeting specific organelles like mitochondria and ribosomes. They discover a peptide ligand that disrupts ribosomal function, killing cancer cells and reducing cell survival in malignant and non-malignant cells.
Researchers develop new methods for injecting drugs and genetic payloads directly into cancer cells using plasmonic nanobubbles. Delivering chemotherapy with nanobubbles increases efficacy and reduces dosage, targeting single-cell level cancer treatment.
Researchers identified a novel anti-leukemia compound, Lenaldekar, that demonstrates effectiveness in eliminating immature zebrafish T-cells and targeting human T-ALL cell lines. The compound showed promise in treating cells from patients with other leukemias, including those resistant to current therapies.
Researchers discovered that the Nrf2 protein plays a crucial role in protecting cells from oxidative stress, which is often exploited by cancer cells to become resistant to treatment. By selectively inhibiting Nrf2, cancer cells may become more susceptible to chemotherapy and radiation therapy.
Researchers found EPR to be 30-46% better at identifying nonmelanoma skin cancer cases compared to claims data. The study suggests using EPR as an alternative for effectively tracking these cases, potentially improving disease burden estimates.
Researchers propose that non-genetic resistance can occur before genetic mutations, changing the approach to designing combination therapies. This new perspective aims to improve outcomes by understanding how cancers evolve and adapt to extreme challenges.
A new drug developed by Northwestern Medicine scientists has prevented human prostate cancer cells from spreading to other tissues. The drug inhibits movement of the cells and prevents metastasis without causing harm to normal cells or tissues.
Scientists have identified PRC2, a chromatin regulator, as a promising therapeutic target in acute myeloid leukemia. Blocking PRC2 halts uncontrolled proliferation and reactivates anti-tumor pathways, offering a potential new treatment option.
Scientists will investigate the role of Myc oncoproteins and a specific mRNA-binding protein, TTP, in controlling tumor growth. The study aims to define mechanisms that could lead to the development of new anti-cancer drugs.
New cell printing technology enables precise pattern formation of human cells, paving the way for advancement in tissue engineering and regeneration. Researchers demonstrated the use of acoustic droplet ejection followed by aqueous two-phase exclusion patterning to control cell placement.
Researchers propose that quantum metabolism explains metabolic changes causing healthy cells to become cancerous, enabling cells to outcompete for space and nutrients. Understanding this process could lead to new cancer treatment approaches.
Researchers developed a new pulsed photoacoustic technique to detect a small number of cancer cells in vitro. The technique combines high optical contrast with high resolution, allowing for the detection of single cancer cells.
Researchers at Queen Mary University of London have identified a mechanism by which normal cells can become cancerous. By understanding how the FOXM1 gene influences cell behavior, scientists may be able to develop new diagnostic tests to detect cancer at an early stage.
Researchers have discovered that a specific protein called p21 can kill certain cancer cells, including sarcomas, by sensitizing their mitochondria to oxidants. This finding provides a rationale for testing existing drugs that increase p21 levels in these types of cancers.
Researchers aim to create targeted compounds that selectively attack cancerous cells by zeroing-in on pollutants produced by tumors' characteristic metabolism. This approach seeks to minimize side effects associated with conventional chemotherapy.
Researchers discovered a two-step ritual in which RNA telomerase partners are prepared for interaction, revealing novel pharmaceutical approaches to cancer and diseases of aging. The study sheds light on the complex process of telomerase biogenesis and its connection to seemingly unrelated diseases.
Researchers at Stanford University have directly observed plasmon resonances in individual metal particles measuring down to one nanometer in diameter. This discovery could lead to advancements in catalytic processes, cancer research and treatment, and quantum computing.
Researchers say forcing dying cancer cells to trigger an immune response could prevent cancer relapses and improve treatment benefits. The new strategy focuses on autophagy, a process that alerts the immune system to foreign invaders.
Researchers found that adding RNAi to standard TKI or antibody therapy can enhance the effect of therapy on NSCLC cell death and slow cell growth. The treatment may benefit patients with EGFR mutations who do not respond to TKI, or those whose cancer is driven by overactive EGFR production.
Researchers at Sanford-Burnham Medical Research Institute found that MLN4924-resistant cancer cells escape death due to a simple mutation in the NEDD8-activating enzyme. The team developed a method to predict how cancer patients will respond to this drug, providing a new path toward personalized medicine.
Scientists have successfully mapped tens of thousands of molecular signaling events involved in DNA damage repair, shedding light on how cells communicate when their DNA is broken. This research will help develop new drugs with fewer side effects and better protect healthy cells during cancer treatment.
Researchers sequenced DNA from cancer cells in patients with myelodysplastic syndromes who later developed leukemia, finding that the disease is an early form of cancer. The study suggests that targeted cancer drugs should be aimed at mutations that develop early in the disease.
Researchers at RIKEN successfully developed a new experimental technique for producing cells with specific functions by reconstructing transcriptional regulatory networks. This technique enables faster and more efficient production of functional cells for cancer therapy and other applications.
A recent study found that the protein Mer resides in the nucleus of leukemia cells, suggesting it may influence gene expression and contribute to cancer development. This discovery opens up new avenues for targeted treatments and potentially more accurate diagnoses.
A major study published in the Journal of Clinical Investigation has identified a method to stop bladder cancer from metastasizing to the lungs. The study found that adding the protein RhoGDI2 to tumors reduces versican production, blocking the ability of cancer cells to grow in the lungs.
Researchers found that telomeres send out a molecular SOS signal when cells take too long to divide, leading to the activation of DNA damage pathways and cell death. This discovery has implications for cancer chemotherapy, suggesting ways to make therapy more potent by combining mitotic inhibitors with other drugs.
Researchers at Weill Cornell Medical College have developed a new tool to image small-molecule metabolites in living cells, offering clues about how to treat disorders. The technology uses modified RNA called 'Spinach' to sense levels of target metabolites in real-time.
Cancer cells use an 'emergency brake' to protect themselves from chemotherapy drugs, which can be rendered inoperative by targeting a specific enzyme pathway. The study identifies PARP inhibition as a promising therapeutic approach to improve chemotherapy effectiveness.
Researchers found that a protein called FOXM1 protects cancer cells from chemotherapy and radiation-induced cell death. Combining standard drugs with proteasome inhibitors may improve treatment effectiveness.
A team from UNC Chapel Hill discovered how a long-studied protein complex influences cell movement and how cells respond to external cues. Cells without the protein complex exhibit altered structure and movement, affecting their ability to sense chemical cues and navigate surfaces.
A phase I clinical trial of patients with advanced pancreatic cancer showed promise with rigosertib, achieving stable disease in 11 of 19 patients for a median duration of 113 days. The drug targets PLK1 and PI3K signals that allow cancer cells to divide rapidly.
Researchers developed a novel technique to turn immune system killer T cells into more effective weapons by delivering DNA into instructor cells. The method proved effective in jumpstarting defective immune systems in immuno-compromised mice and human killer T cells, paving the way for potential cancer therapy.
Researchers at Harvard's Wyss Institute have developed a DNA nanorobot that can seek out specific cell targets and deliver molecular instructions to cause cancer cells to self-destruct. The technology uses modular components to mimic the body's immune system and has the potential to treat various diseases.
Researchers used Hi-C technology to generate a 3D model of a mouse genome and mapped chromosomal breaks to explore the impact of spatial proximity on reassembly. The study found that breaks near each other were more likely to be incorrectly attached to neighboring chromosomes.
Researchers at Yale University have identified a new regulator that controls p53's activity in sperm production, which could lead to breakthroughs in fertility treatments and cancer therapy. The study found that a molecule called Pumilo 1 plays a crucial role in this process.
Researchers have gained a better understanding of two key proteins that control cell division, which could lead to the development of new drugs to stop cancerous cells multiplying. This discovery could also help optimise personalised chemotherapy treatments and limit side effects associated with some chemotherapy drugs.
Scientists discovered that T cells can temporarily lose their ability to fight cancer when exposed to self-antigens, but return to normal function under certain conditions. Researchers hope to develop new cancer therapies by understanding and overcoming this tolerance mechanism.
Researchers discovered that nonsteroidal anti-inflammatory drugs (NSAIDS) inhibit tumor metastasis by reducing lymphatic vessel dilation and prostaglandin pathways. This mechanism provides a potential target for cancer treatment.
Researchers at the University of Washington have developed a new method to stimulate neurons in the brain using quantum dots. This technique allows for precise control over cell activity and could provide insights into disease processes and potential treatments for conditions like Parkinson's disease, Alzheimer's, and severe depression.
Monocytes are extremely sensitive to reactive oxygen species (ROS), while macrophages and dendritic cells derived from monocytes are resistant due to their defective DNA repair mechanisms. This sensitivity may play a role in regulating the immune response and preventing excessive ROS production.
Cell biologists have identified key steps in how small molecules alter a cell's skeletal shape and drive cell movement. By manipulating the cell membrane, researchers created ruffles that helped pull cells across surfaces, a process previously difficult to recreate.
Researchers have developed a novel technology platform that enables viewing of biological processes in dynamic, life-sustaining liquid environments. This innovation allows for high-resolution imaging of cancer cells and other macromolecules, providing new targets for drug therapy.
Researchers at the Translational Genomics Research Institute and University of Arizona have received a grant to study targeted cancer therapies for pancreatic cancer, which shows promise in reducing side effects. The center aims to develop novel antitumor agents that can extend the productive lives of patients with cancer.
Ziv Bar-Joseph, a Carnegie Mellon University professor, has received the Overton Prize for his outstanding contributions to computational biology. He has made significant breakthroughs in gene regulatory networks and their applications to cancer cells.
Researchers found grape seed extract to be effective in killing head and neck squamous cell carcinoma cells without harming healthy cells. The extract damages cancer cells' DNA and prevents repair pathways from functioning.
A study published in The Journal of Cell Biology reveals how DGK-alpha, a lipid-converting enzyme, enables invasive cancer cells to recycle integrins, providing better traction on fibronectin fibers. This process is essential for tumor progression and metastasis.
Research by Michael Goldberg and Phillip Sharp found that selectively inhibiting PKM2 can kill cancer cells by depleting energy sources. This approach has shown promise in regressing established tumors in mice, suggesting a potential strategy against various cancers.
Scientists found that caffeoylquinic acid derivatives from mate tea induce apoptosis in human colon cancer cells, reducing markers of inflammation. The study suggests mate tea has potential as an anti-cancer agent and may be beneficial for other diseases associated with inflammation.
Researchers have discovered that luteolin, a flavonoid found in fruit and vegetables, can inhibit the activity of cell signaling pathways important for colon cancer cell growth. This inhibition leads to reduced IGF-II secretion, decreased receptor expression, and ultimately, cell death.
Researchers discovered that the interaction between CD4 T cells and myeloid-derived suppressor cells (MDSC) can inhibit T-cell function, while CD8 T cells are not affected. The study suggests a potential mechanism for controlling dysregulated immune responses in cancer.
A faulty version of the RHBDF2 gene is responsible for tylosis with oesophageal cancer, a rare inherited condition. The study reveals that this gene malfunction leads to uncontrolled cell growth and division, causing cancer.