Articles tagged with Cancer Cells
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Researchers discovered that lung cancer cells switch to using amino acid glutamine when glucose is scarce, allowing them to continue growing under starvation conditions. Blocking this enzyme PEPCK could slow tumor growth in mice, suggesting a promising new approach to treating non-small cell lung cancer.
Researchers at Emory University's Winship Cancer Institute have discovered a potential anticancer drug in orange lichens, called parietin. The pigment kills human leukemia cells and inhibits the growth of cancer cell lines, including lung and head and neck tumors.
The Blue Brain Project digitally reconstructs a slice of juvenile rat brain containing over 31,000 neurons and 55 layers, enabling researchers to simulate neural activity and circuit-level behaviors
Researchers discovered that intracellular receptor signalling sustains cancer cells detached from surrounding tissue. Preventing this signalling reduces the ability of cancer cells to survive and spread. This breakthrough opens a new perspective on integrin receptors' activity in cancer.
A team of researchers from Oxford University has identified a protein called PAT4 that tumours use to detect food supplies. Targeting this protein may restrict cancerous cells' ability to grow and improve survival rates.
Researchers have discovered a new molecular marker for killer cells, allowing for the prediction of infection course. The marker, CX3CR1 receptor, is associated with chronic infections, where immune system effectiveness is compromised.
Researchers discovered a method to reprogram fibroblasts, healthy tissue around tumors, to trap and contain cancer cells. This approach reduces the movement of cancer cells away from the tumor, showing promise in preventing tumor spread. The study has potential for various cancer types and could lead to better ways to control the disease.
A new study by the University of Copenhagen and Cancer Research UK shows that targeting fibroblasts can block cancer cell movement, trapping them in healthy tissue. The research uses a drug that targets PHD2, an inhibitor currently in clinical trials for anaemia.
The BGU project Boomerang is a modular system that recognizes cancer cells at a high level of specificity and can cause disruption of genes essential for cancer survival or activate suicide genes. It has many applications in personalized medicine, paving the way to change the approach to cancer treatments.
Researchers at Harvard University have discovered a molecule that can halt the growth of cancerous AML cells without harming healthy cells. The molecule, cortistatin A, works by inhibiting two specific kinases that play a key role in the growth of AML cells.
The CheckMate 057 trial shows that nivolumab improves overall and 12-month survival rates compared to docetaxel in non-squamous non-small cell lung cancer patients. Nivolumab also demonstrated better patient-reported outcomes, including quality of life and slower disease deterioration.
Researchers have identified GATA4 as a key transcription factor that activates cellular senescence. This process is characterized by a pro-inflammatory response and the production of secreted inflammatory cytokines. The study reveals that GATA4 is normally suppressed by autophagy, but its accumulation promotes senescence.
A new methodology allows for the tracking of DNA methylation patterns in individual cells over time, providing insights into gene expression and cell identity. This breakthrough could aid in cancer treatment and other diseases by identifying specific genes to activate or silence.
A new metal-based compound, Compound 5, has been developed to destroy kidney cancer cells while leaving normal cells unharmed. The compound, which incorporates both titanium and gold, has shown excellent promise in pre-clinical models, outperforming the FDA-approved drug Cisplatin.
Researchers have identified a key role for the WWOX gene in suppressing cancer development. Lower levels of WWOX are associated with more aggressive and treatment-resistant cancers. The study suggests that targeting the enzyme activity of WWOX could influence cancer cell properties.
A Stanford team re-engineered a virus to create a smart particle that can deliver therapeutic payloads to specific cells. By adding molecular tags, the particles can target diseased areas while leaving healthy tissue alone.
A modular system of proteins can detect a specific DNA sequence in a cell and trigger a response, such as cell death. The system can be customized to detect any DNA sequence and trigger a desired response, including killing cancer cells or cells infected with a virus.
UAB researchers discovered a triple mechanism that stops chromosome separation in response to DNA injuries, preventing cancerous transformation. The three control pathways, mediated by genes Wee1, Pds1/securina and Rad53/Chk2, must be eliminated simultaneously for damaged chromosomes to be segregated.
A research team at Northwestern University has developed a computational algorithm that leverages cells' noisy nature to control the networks governing cellular behavior. By controlling a smaller network of state transitions, they can promote cellular health and prevent disease.
Researchers found that Myc oncogene disrupts circadian rhythm and metabolism in cancer cells by promoting REV-ERBα activity, leading to poor clinical outcomes. Inhibiting REV-ERBα may partially rescue disrupted circadian oscillations and improve treatment effectiveness.
Cancer Research UK scientists found that some cancer cells can survive gene damage caused by HDAC inhibitor drugs, triggering a 'survival' response. This mechanism rebalances tags and maintains normal gene activity, making it harder for the drug to kill cancer cells.
Cancer patients who receive chemotherapy treatment for a sustained period have heightened levels of reactive oxygen species (ROS), which correlates with drug resistance. The study proposes a measure of relative ROS levels under normal conditions to help determine if patients are becoming resistant to cancer drugs.
Scientists have identified a FOXC1 gene that causes more aggressive cancer in AML patients. When switched on in blood cell tissue, it stunts the development of blood cells and stops them maturing into normal specialized blood cells, leading to faster cancer growth.
Researchers at Imperial College London have created a fluorescent molecule that can reveal the presence of quadruplexes in living cells. This breakthrough could be a game changer to accelerate research into these DNA structures and identify new compounds that can bind to them, potentially leading to new cancer treatments.
A new method of harvesting and growing lung stem cells has been developed by researchers at NC State University, which could provide an effective treatment for idiopathic pulmonary fibrosis (IPF). The study used a multicellular spheroid environment to enrich adult lung stem cells, which showed promise in mice trials with reduced inflam...
Researchers discovered how capsaicin interacts with cell membranes, finding that it lodges near the surface and can cause membranes to come apart. This insight may lead to novel tools against cancer or other conditions. The study appeared in ACS' The Journal of Physical Chemistry B.
A team of researchers has identified a new role for the RAB35 protein in cancer development, finding that it stimulates key growth-control pathways and can transform normal cells into cancerous ones. The study suggests that dysregulated membrane trafficking may play an important role in oncogenesis.
A clinical trial of a personalized cell therapy, CTL019, achieved an overall response rate of 57% and complete remissions in eight out of 14 patients with chronic lymphocytic leukemia (CLL). The therapy, developed by Penn researchers, involves reprogramming patients' own T cells to hunt and kill cancer cells.
Researchers discover that altering protein recycling complexes in human cells enables cancer cells to resist treatment with proteasome inhibitors, a class of drugs used to kill cancer cells. The discovery highlights the potential for targeting this resistant state to develop new cancer treatments.
Researchers found that Brazilian wasp venom's MP1 toxin selectively kills cancer cells by interacting with abnormally distributed lipids on their surface. The peptide creates gaping holes, allowing critical molecules to escape and potentially leading to new anticancer drug development.
Cancer cells can be made vulnerable to autophagy shutdown by combining an FLT3 inhibitor with an autophagy blocker. This combination prevents cancer cells from metabolizing glucose and mobilizing stored nutrients, leading to cell death. The study provides evidence that this approach could be a new way to treat various types of cancer.
Researchers find that using a monoclonal antibody to block the 'eat me' signal on malignant cells triggers a more potent immune response in dendritic cells, which then activate killer T cells and boost adaptive immunity. The study suggests a new approach for developing an effective cancer immunotherapy.
Scientists have created a nanoscale vehicle made of DNA to shuttle the CRISPR-Cas9 gene-editing tool into cells. This 'nanoclew' ensures precise control over the dosage of editing, reducing unintended edits. The researchers successfully tested the system in cancer cell cultures and tumors in mice, achieving promising results.
Researchers at the Salk Institute have identified a critical difference in how cells respond to DNA breaks versus viral infections. The discovery reveals that cells can selectively neutralize viral DNA without triggering a global response, which could lead to the development of new cancer-selective viral therapies.
Researchers at the University of Texas Health Science Center have identified a new electrical mechanism that controls molecular switches regulating cell growth. The study focuses on K-Ras mutations found in 20% of human cancers, which can lead to uncontrolled cell division and cancer.
Researchers at Florida State University have identified a protein called Treslin that shows promise in stopping the unregulated division of cancer cells. Treslin stimulates the activation of helicase, a key enzyme involved in DNA replication, and assembles it for cell division.
Scientists at Emory University School of Medicine found that alpha lipoic acid can stimulate telomerase, the enzyme that lengthens telomeres, with positive effects in a mouse model of atherosclerosis. The discovery highlights a potential avenue for treating chronic diseases.
Researchers in China have developed tiny nanocrystals that can specifically target and identify cancer cells, potentially leading to earlier diagnosis and treatment. The nanocrystals, made from heavy metals lanthanum and europium, can be used as 'staining' agents to highlight diseased cells under a microscope.
Researchers found that tubulin assembly involves a single machine comprising the largest four genes, which powers the process using chemical energy and assembles microtubules that play critical roles in cell structure and division. Understanding this system may provide new strategies for controlling microtubules in cancer cells.
Researchers at VIB and KU Leuven found that inhibiting PHD1 prevents p53 activation, leading to improved response to chemotherapy in colorectal cancer cells. This discovery offers new therapeutic potential for increasing sensitivity to chemotherapeutic treatments.
Researchers found that ribosomes can translate the 'untranslated region' of mRNA, producing small proteins whose functions are unknown. This discovery opens up new questions about cancer cell growth and how cells respond to stress.
Researchers found that malaria infections cause widespread DNA damage in B lymphocytes, increasing the risk of blood cancers. Chronic inflammation from malaria promotes genomic instability, leading to mutations and cancerous changes.
Researchers at Oregon State University have made a significant advance in photodynamic therapy to combat ovarian cancer, achieving complete cancer cell elimination with no regrowth of tumors. The new approach combines existing techniques with compounds that make cancer cells vulnerable to reactive oxygen species, reducing natural defen...
Researchers have developed a yeast model to investigate a gene mutation that causes massive DNA damage and allows cells to continue dividing. The study reveals how cells ignore genetic damage and form micronuclei, which are commonly found in cancer cells.
Worcester Polytechnic Institute researcher Amity Manning is awarded $747,000 from the National Institutes of Health to explore molecular mechanisms driving genetic instability in cancer cells. The goal is to turn the genetic tables against cancer by understanding how specific molecules affect DNA packaging and organization.
Researchers have discovered that protein Hsp90 triggers cancer cell metabolism, providing a potential therapeutic target. The modified protein is toxic to cells in neurodegenerative disorders but acts as a pro-survival agent in tumor cells.
Researchers developed a biosensor to measure Mitochondrial Pyruvate Carrier (MPC) activity in malignant cells, finding low MPC activity compared to healthy cells. Treating cancer cells with a new compound restored normal MPC activity, suggesting the carrier's dysfunction is responsible for its inactivity.
A phase 1 trial demonstrates the safety and effectiveness of resiquimod gel in treating early-stage cutaneous T cell lymphoma, causing regression of both treated and untreated tumor lesions. The treatment also enhances immune response, leading to healing of even untreated lesions.
ATF3 is a critical protein that helps repair DNA damage and prevent cancer. When cells experience stress, ATF3 binds to the Tip60 protein, promoting DNA repair and cell response. The study suggests that increasing ATF3 levels could lead to new cancer therapies.
A novel combination of techniques is used to create a biocompatible nanodevice that can deliver localized heating to cancer cells while accurately sensing temperature with diamond nanocrystals. This allows for precise targeting of biological molecules and effective thermal cancer therapy.
Researchers develop novel imaging technology to visualize brain's intricate structures, including neurons and blood vessels. The breakthrough enables scientists to study neurological disorders and understand how brain development shapes individual identity.
A team of international scientists decoded the molecular characteristics of a fatal subtype of leukemia in children, paving the way for new therapeutic approaches. The study identified genetic aberrations and altered gene expression programs that lead to tumorigenesis, providing potential druggable targets.
Researchers discovered that a protein imbalance, specifically between Plcγ1 and Grb2, can lead to cell proliferation and cancer formation. High levels of Grb2 relative to Plcγ1 are associated with a favorable prognosis in ovarian cancer patients.
Researchers at the University of Toronto have discovered a motor protein complex that transports severely damaged DNA within cells. The discovery sheds light on how cancer operates and could lead to new anti-cancer drug targets.
Researchers discovered that cancer cells incorporate chemically modified nucleosides into their DNA, which is toxic to them. The study found that modifying these nucleosides could be used as a specific anti-cancer agent, exploiting epigenetic changes in cancer cells.
A RIKEN-led team has developed a large-scale map of primary cell-to-cell interactions, revealing common signaling routes between cells and new insights into receptor evolution. This data can contribute to the development of medical treatments by identifying potential targets for therapies in various diseases.
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.
A team of Canadian and British researchers has made a breakthrough discovery about the cell division mechanism, finding that chromosomes emit signals to influence microtubule action. This signaling pathway is crucial for the segregation of chromosomes during cytokinesis, a critical step in cell division.
Researchers have developed a new cancer drug FY26 that is 49 times more potent than Cisplatin, effectively shutting down the metabolism of cancer cells. The drug works by forcing cancer cells to use their mitochondria, which are defective in healthy cells, leading to cell death.
Research from the University of Cambridge found that exhausted immune cells are bad news for infections, but good news for autoimmune diseases like lupus and Crohn's disease. The study suggests that targeting T cell exhaustion could lead to more effective treatments for these conditions.