Research on the cell biology of tumors. Covers cancer-cell vulnerabilities, tumor spread, nanoreactor therapies, and AI-guided cancer research.
Researchers have developed a biomaterials-based system that uses soft microfibers to activate and expand T cells, increasing their number by nearly an order of magnitude. This approach simplifies processing compared to existing systems and has the potential to bring new hope to cancer patients for T-cell therapy.
Conventional cancer therapy can create an inflammatory cascade in the body, leading to aggressive tumor progression and recurrence. However, resolvins have been shown to counteract these effects, enhancing the body's clearance of cell debris and reducing tumor growth.
Researchers used Cryo-EM to capture images of molecular machinery called RNA Polymerase III in unprecedented detail, revealing five key stages in which the complex reshapes itself to successfully transcribe the DNA code. This discovery could open up new approaches to cancer treatment by targeting the complex's activity.
A team of researchers has developed an innovative approach to remotely control genetic processes in live immune T cells, enabling them to recognize and kill cancer cells. The system uses mechanogenetics to convert mechanical signals into genetic control, with potential to increase precision and efficiency in CAR-T cell immunotherapy.
A team of cancer researchers has made a significant contribution to our understanding of cancer cell regulation, which could lead to improved cancer treatments. The study focuses on kinases, proteins that influence cancer cell growth and development, and identifies new strategies for killing cancer cells.
Researchers at the University of Warwick have developed a new line of attack against cancer using an organic-osmium compound, JPC11, which targets a metabolic process relied on by cancer cells. The treatment can be recycled and reused within cancer cells to attack them repeatedly.
Researchers at Cold Spring Harbor Laboratory have developed a method to selectively disable the MYB protein, which enables cancer cells to proliferate. In tests in mice, this approach resulted in an 80% reduction in size of aggressive leukemia without harming normal cells.
Researchers found combining blueberry extract with radiation increases treatment effectiveness for late-stage cervical cancer, reducing healthy cell damage by up to 70%. The study's lead author suggests blueberries as a potential radiosensitizer, a non-toxic chemical that enhances cancer cells' responsiveness to radiation therapy.
Researchers found a novel combination of PARP and BET inhibitors to be effective in treating ovarian cancers without BRCA1 and BRCA2 gene mutations. The combination resulted in enhanced sensitivity of cells to cell death, offering potential applications in broadening treatment options for various malignancies.
Researchers measured absolute cross sections for secondary electrons interacting with DNA molecules in a condensed-phase environment. This study provides insights into the damage and radiation dose delivered to patients in radiotherapy.
Researchers have measured and mapped the key molecular forces on platelets that trigger blood clotting. The findings suggest that platelets care about the direction of forces applied to them, requiring a lateral force signal to prevent unnecessary clotting.
Scientists at The Ottawa Hospital and University of Ottawa discover Maraba virus can eliminate latent HIV-infected cells. Laboratory tests show the virus targets cells with impaired interferon pathway, leaving healthy cells unharmed.
A KAIST research team developed technology to identify the optimal drug target for cancer cells based on molecular network dynamics. This approach uses systems biology to analyze genetic mutations and predict drug response, which could lead to more effective treatment strategies.
Researchers at the University of Copenhagen have discovered a new mechanism by which cancer-inhibiting proteins regulate signaling molecules. The study found that primary cilia, or cellular antennae, play a crucial role in balancing PDGFRα signaling, preventing excessive receptor activation that can lead to brain and gastrointestinal t...
Researchers at UNC School of Medicine discovered that the minichromosome maintenance (MCM) complex plays a crucial role in keeping stem cells in their immature state. The study suggests that rapid MCM loading rate is essential for maintaining stem cell identity.
A new study reveals that mutations in 'Ras' genes, which drive 25% of human cancers, can also suppress the immune system around tumors by increasing PD-L1 levels. This understanding will help offer patients more precise and effective treatments.
Researchers at iMM found that certain molecular signals allow cancer cells to survive chemotherapy by altering mitochondrial metabolism. Using VEGF-blocking drugs, they were able to render these cells vulnerable to chemotherapy.
A research team led by Professor Jens Nielsen has mapped out the complex metabolism of yeast cells, enabling the efficient production of protein therapies for diseases like cancer. The breakthrough could lead to significantly cheaper treatments, potentially reducing costs by 10%.
Researchers at German Cancer Research Center prove grid cells measure distances and enable path integration in mice, aiding spatial orientation. This innate behavior helps animals find the most direct route from A to C without learning or visual cues.
A landmark clinical trial has shown impressive results for a CAR-T cancer treatment in refractory large B-cell lymphoma patients, achieving complete remission in 42% of cases. However, severe side effects including cytokine release syndrome and neurologic problems were also observed, affecting up to 95% of patients.
A Phase 1 trial of the targeted agent BLU-285 demonstrated rapid and durable responses with minimal adverse effects in patients with advanced systemic mastocytosis. The study found that 72% of evaluable patients achieved an overall response, with 100% having disease control.
Researchers found that leftover cancer cell debris can stimulate tumor growth, but resolvins can block this response. The study suggests a new approach to enhance cancer therapy and prevent recurrence.
Researchers found that ERK activity propagates as a wave, guiding cells to migrate in the opposite direction. This mechanism may be used to suppress cancer cell infiltration.
Researchers found that SIRT1 stabilizes a mechanism preventing immune cell toxic effects, but its loss accelerates glycolysis and cytokine production. This understanding led to potential new drug targets to strengthen or weaken SIRT1, potentially countering age-related diseases.
Researchers identify a fleeting, yet key structure that allows cells to break through tissues and spread to other parts of the body. A single protrusion bulges out from the cell surface, wedges a hole through the protective layer, and swells until the breach is wide enough for the entire cell to squeeze through.
Researchers at Cardiff University have developed a new method of engineering T-cells to attack cancer using CRISPR genome editing. This breakthrough enhances the T-cells' ability to recognize specific cancer cells and destroy them, offering new hope in the fight against various types of cancers.
Researchers discovered that tumor metabolism damages naïve T-cells, affecting cancer immunity and immunotherapy. The study suggests targeting lactate pathway to improve immunotherapy effectiveness.
Scientists at NIST have discovered a way to make tiny colonies of cells grow in three-dimensional structures inside petri dishes, paving the way for more realistic biological environments for testing pharmaceuticals. The method could help bridge the gap between lab and living creature testing, speeding up drug development.
Researchers at the University of Bergen find that NTZ deactivates activated Beta-catenin in prostate and colon cancer cells, stopping their growth. The discovery could lead to faster development of new treatments for these cancers.
Researchers have developed a molecular sensor that can detect and eliminate cells with mutated TP53 genes, which are responsible for 50% of all human tumors. The sensor initiates cell death if the gene is non-functional, preventing tumor formation at an early stage.
Researchers have created an artificial protein that inhibits G protein activators, leading to the potential blockage of malignant properties in cancer cells and correction of birth defects. The findings may pave the way for identifying new molecular targets for therapeutic intervention.
Researchers discovered that T cells can thrive in oxygen-depleted environments when equipped with growth factor VEGF-A. This adaptation allows them to kill cancer cells more effectively, contrary to previous assumptions.
Scientists mapped the flow and regulation of nucleotides, revealing a mechanism that slows down DNA replication when out of rhythm. This slowdown allows for nucleotide production to catch up, ensuring healthy genome copying without mistakes.
Researchers at KU Leuven unravelled how the cell division timer is switched on and off, potentially leading to effective cancer therapy. The discovery involves a biochemical clock that gives cells time to fix attachment-related problems, allowing for more efficient cell division.
Researchers develop a new strategy for treating cancer by controlling chromatin packing densities, which determines gene expression and resistance to treatment. The approach has shown promising results in cellular cultures and is now being tested in animal models.
Researchers discover iridium, a densest metal, kills cancer cells by filling them with deadly oxygen, without harming healthy tissue. The treatment uses laser light to activate the compound, targeting key proteins in cancer cells.
Researchers at the University of Arizona found that even with perfect natural selection, aging would still occur due to cancer cells cheating the system. Slowing down one type of cell can lead to an increase in another problematic cell type, making it mathematically impossible to halt aging.
Treg cells suppress immune function, but eliminating them doesn't eliminate their effects. In fact, dying Tregs release metabolites that affect T-cells, making them unhealthy and reducing the cancer-fighting effect of immunotherapy. The study suggests a new approach to limit this function and block the suppressive activity.
Researchers at the University of Zurich have discovered a crucial mechanism for epigenetic gene regulation, involving the DNMT3A enzyme. This finding provides new insights into the development of aggressive types of leukemia and may lead to more effective treatments.
Researchers discovered that the timing of DNA damage within cell cycle phases affects a cell's fate, with certain stages vulnerable to DNA damage. The study suggests that synchronizing cancer cells in susceptible phases before treatment could be an effective strategy.
Researchers identified NOX4 enzyme as a key mechanism in kidney cancer recurrence, finding it facilitates survival of cancer cells under drug treatment. The study's findings have potential for developing targeted therapies to reverse the mechanism and prevent further disease progression.
Researchers at Northwestern University have discovered a novel form of cancer therapy using RNA molecules that trigger self-destruction in cancer cells. The mechanism, called DISE, eliminates multiple genes required for cell survival, making cancer cells resistant to treatment.
Researchers found that on average, one to ten driver mutations are required for cancer to emerge. The study also reveals the number of mutations driving cancer varies considerably across different cancer types. By using an evolutionary approach, scientists can identify key genes and mutations involved in cancer evolution.
A new synthetic compound, E260, has been developed to target the energy generation system of cancer cells, inhibiting an enzyme that supports their survival and dissemination. This approach has shown promising results in treating mice with metastatic cancer, completely curing them with no toxic effects.
A new study suggests that many pelvic tumors in women may have a common origin in the fallopian tubes, which could lead to new strategies for preventing and early detecting ovarian cancer. The research found that ovarian cancer cells share genetic similarities with cells covering the tips of fallopian tubes.
A new study reveals that cancer cells can use the body's own immune system to wake themselves up and fuel their growth after treatment, leading to relapse. Researchers found that immunotherapies targeting this response could delay or prevent cancer return in mice, suggesting a promising approach for patients at risk of relapse.
Researchers found a link between sugar consumption and cancer development through yeast cell research, clarifying the Warburg effect. The study suggests that high sugar metabolism in cancer cells stimulates tumor growth.
Researchers found over 30,000 publications reporting on misidentified HeLa cells, leading to potentially invalid research data and reproduced results. The study aims to raise awareness about the problem and promote caution when interpreting results.
Researchers at RIKEN discovered a way to prevent liver cancer spread by treating with a modified fucose sugar. The treatment disrupts biological pathways, blocking hepatoma cells from invading healthy liver cells and suppressing migration, but not proliferation.
Scientists at Goethe University Frankfurt reveal how correct molecular passports are selected by cells to avoid autoimmune diseases and cancer. The new discovery sheds light on the quality control of antigens, crucial for effective immune surveillance.
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.
A new computer program called SCENIC enables researchers to quickly and accurately identify different cell types in the human body. The method helps understand how cell fate is regulated and could lead to the discovery of master regulators and potential drug targets.
Scientists at Albert Einstein College of Medicine have discovered a compound that directly makes cancer cells commit suicide while sparing healthy cells. The new treatment approach, BTSA1, works by triggering apoptosis in cancer cells through the BAX protein, leaving healthy cells unscathed.
Researchers found that a protein named ZATT can eliminate DPCs with the help of another protein TDP2. Understanding how TDP2 and ZATT work together may improve cancer patient health outcomes. The discovery could lead to development of new drugs targeting these defenses.
Researchers found that cancer cells 'recharge' by transferring power-generating mitochondria from healthy bone marrow cells, supporting leukaemia growth. Inhibiting a specific enzyme reduced mitochondrial transfer and slowed cancer growth.
New research explains why mTOR inhibitors can't fully eliminate cancer cells. The drugs target a cell regulator called mTOR, which controls mitochondrial structure and function, ultimately protecting cells from death.
Researchers discovered how TORC1 protein complexes regulate cell growth in response to sugar availability. In the absence of sugar, these complexes self-assemble into massive tubular structures that halt cell growth. The formation and disassembly of these tubules can be easily observed in living cells.
Researchers discovered that chromatin fragments outside the nucleus activate a DNA-sensing pathway, leading to chronic inflammation and tissue damage. The study aims to develop small molecules targeting this inflammatory pathway to treat age-related diseases.
Researchers have identified a distinctive epigenetic event in immune cells that differentiate in the tumoral microenvironment, making them tolerant to cancer cells. The study found that DNA methyltransferase 3A is responsible for the acquisition of suppressive properties in these cells.
Researchers have engineered smart protein molecules called iSNAPS that can rewire macrophages to ignore a 'don't eat me' signal from cancer cells, allowing them to engulf and destroy cancer cells. This breakthrough could lead to a new method of re-engineering immune cells to fight cancer and infectious diseases.