Articles tagged with Tumor Cells
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Researchers have successfully combined an antibody-drug conjugate with immunotherapy to treat breast cancer. The therapy has shown promising results in attacking tumor cells and improving the body's immune response.
Researchers describe a new treatment option for glioblastoma multiforme, targeting malignant cells while leaving healthy cells alive with high-frequency pulsed electric fields. The therapy has shown promise in killing tumor cells by disrupting cell membranes and causing nuclear collapse.
A team of U of T engineers has developed a way to grow cancer cells in the form of a rolled-up sheet that mimics the 3D environment of a tumour, offering a way to speed up drug development and ask new questions about cell behavior. The single-layer design makes it easier for other lab researchers to adopt the process.
A new study by Siyuan Zhang and colleagues reveals that the microenvironment of tumor cells has a significant impact on cancer metastasis. The study suggests that the 'seed and soil' model, where tumors adapt to new tissues, can be used to prevent metastasis.
Researchers from NTU Singapore have successfully used dead bacteria to destroy colon tumour cells effectively. The study published in Scientific Reports shows that the secretions of dead Clostridium sporogenes bacteria can reduce the growth of colorectal cancer cells by up to 83%.
Researchers discovered brain cancer cells form a complex network to resist treatment and invade healthy brain tissue. The tumor cells use this network to communicate and repair damage, making it resistant to radiation therapy.
PharmaMar's novel Antibody-Drug Conjugate (ADC) MI130004 demonstrates potent anticancer activity against HER2-expressing breast, gastric, and ovarian cancers. The ADC impairs tubulin polymerization, causing mitotic failures and halting cell division in tumor cells.
A TSRI team has been awarded a $1.8 million grant to investigate the molecular mechanisms behind cancer metastasis. The research could lead to new approaches to help patients by targeting specific molecules involved in tumor cell survival and metastasis.
A new study from TSRI found that high levels of epidermal growth factor receptor (EGFR) encourage blood vessel growth in early tumor development, facilitating cancer cell dissemination and metastasis. The findings highlight the urgent need for new methods to diagnose cancers early and new treatments to fight growing metastases.
Researchers found that patrolling monocytes play a key role in blocking lung metastasis by recognizing and scavenging tumor cells. This discovery could lead to new treatments for lung cancer by augmenting existing immunotherapy approaches.
Researchers found that tumor suppressor protein PTEN is lost in brain cancer cells but restored once they migrate to other organs. This reversible loss enables brain metastases growth and protects against cell death.
A long-known tumor suppressor, pRb, works by restricting the activity of KDM5A, a molecule that regulates fuel burning in mitochondria. Cancer cells rely on fermenting sugars for energy, making them more vulnerable to metabolic therapies.
A team of researchers is using the Cray XK7 Titan supercomputer to simulate hundreds of millions of red blood cells in an attempt to develop better drug delivery methods and predictors for diseases like sickle cell anemia. The simulations are focused on understanding how these diseases interact with human blood vessels, particularly in...
Researchers have found a way to mobilize immune cells to attack and destroy malignant tumors by using a cell surface receptor called GITR. This protein can switch immature T-cells from becoming regulatory T-cells to tumor killers called Th9 cells, which produce the cancer-fighting protein interleukin 9.
Researchers discovered that cell programs controlling normal mammary gland stem cells differ from those regulating cancer stem cells, which arise in a distinct layer of tissue. This finding could lead to new cancer treatments by targeting the specific differences between normal and cancer cells.
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 found a core group of genes related to both viral defense and susceptibility to demethylating drug 5-azacytidine. The study suggests that triggering this pathway may improve the effectiveness of immunotherapy drugs in patients with certain types of cancer.
A Harvard University collaboration has developed a 3D model of solid tumors that reflects both their three-dimensional shape and genetic evolution. The model explains why cancer cells share an unusually high number of genetic mutations and how drug resistance evolves, shedding light on tumor growth and evolution.
Computer models of developing cancers show that small cell movements can quickly alter tumor composition. The models suggest treatments targeting these movements could slow disease progress by preventing certain cells from flourishing.
A new minimally invasive vaccine combines cancer cells with immune-enhancing factors, evoking an immune response in a simpler and more economical way. The approach has shown promising results in experimental animal models, shrinking tumors and protecting animals from tumor growth.
Researchers at Mayo Clinic have discovered a way to potentially reprogram cancer cells back to normalcy by restoring the expression of specific microRNAs. This finding represents an unexpected new biology that provides the code for turning off cancer, offering a potential strategy for cancer therapy.
A new study by the University of Pennsylvania School of Medicine has found that tumor cells associated with pancreatic cancer often behave like communities, working together to increase tumor spread and growth. The research suggests that interactions between subpopulations of tumor cell types contribute to metastatic progression.
A new method called Time-lapse Imaging Microscopy in Nanowell Grids (TIMING) allows researchers to study immune cells and cancer cells in isolation, enabling the identification of high-performing outliers. This technology has the potential to expand cancer immunotherapy treatment options for more patients.
A Brazilian antibody developed by Recepta Biopharma with FAPESP support will be used to create a new cancer drug. The technology has been licensed to US-based company Mersana Therapeutics, which will use it to develop an immunoconjugate against target tumor cells.
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.
Researchers discovered that CA125-negative tumor cells have an enhanced ability to repair their DNA and resist programmed cell death, making them dangerous. Combining chemotherapy with birinapant significantly improved disease-free survival in laboratory models of human ovarian cancer.
Researchers at Lawson Health Research Institute have identified LKB1 as a key player in promoting and surviving ovarian cancer cells. This discovery contradicts previous studies, which suggested that LKB1 acts as a tumour suppressor in ovarian cancer.
Researchers at University of Pennsylvania implicated defects in mitochondria as a key factor in cancerous cell transition. Disrupting mitochondrial components led normal cells to adopt cancerous characteristics, including increased glucose consumption and invasive behavior.
Natural killer cells are impaired in the tumor microenvironment, but can be restored in normal conditions. Researchers identified two key factors blocking NK cell function: inflammatory cytokine IL-10 and down-regulated NKG2D ligands.
A recent study discovered that Daple protein is a tumor suppressor in the early stages of colorectal cancer, but may actually facilitate disease spread at later stages. Researchers found that higher levels of Daple were associated with better patient survival rates and lower tumor growth.
Ghajar is investigating two approaches: keeping dormant cells asleep or destroying them altogether to prevent breast cancer metastasis. He aims to identify factors that keep cells asleep and profile molecules that mediate chemo resistance, potentially providing a lasting cure for cancer patients.
Scientists at the Salk Institute discovered that telomeres play a more central role in a self-destruct program in cells that prevents tumors than previously thought. This process, called crisis, can be exploited to improve cancer therapies by targeting telomeres and making cells more susceptible to chemotherapy.
A new study suggests that cell fusion can initiate cancerous processes and tumor formation through 'genomic catastrophe', leading to chromosomal instability and DNA damage. Fused cells from rat intestinal epithelial cells formed tumors in immunodeficient mice, providing evidence for a molecular mechanism driving neoplastic transformation.
The combination of MEDI4736 and tremelimumab has been shown to have manageable toxicity and clinical activity in advanced NSCLC patients, including those with PD-L1 negative tumors. Eight out of 31 evaluable patients achieved a partial response.
Differences in tumor cell metabolism lead to more aggressive behavior in the center of a tumor. Mathematical modeling shows that cells with high glucose metabolism and acid production become invasive and cause tumor recurrence.
Researchers developed a microfluidic device called the Cluster-Chip to capture clusters of two or more cells, which are significantly more likely to cause metastases. The device proved 40-50% better at finding clusters with targeted markers and 1000% better at capturing cells without them.
Dying daughter cells release protein Pvf1, binding to nearby mother stem cells' receptors, preventing apoptosis. This allows stem cells to survive until they can regenerate damaged tissue. The discovery may lead to new cancer treatments by targeting protective signals in tumor-initiating cells.
Scientists at The Wistar Institute have identified a way that cells can reprogram their metabolism to overcome senescence, a tumor-suppressing mechanism. This reprogramming allows for the proliferation of cells that should have become senescent and has the potential to lead to tumor formation.
Researchers at the University of Notre Dame investigate the clinical potential of microvesicles, shedding light on their role in promoting tumor invasion and metastasis. The study identifies key proteins that guide the formation of these vesicles and suggests a potential link to biomarker development.
Researchers have identified a novel approach to treating pancreatic cancer by introducing the protein E47, which can reprogram cancer cells back to their original state. This breakthrough offers new therapeutic possibilities and may lead to improved patient outcomes.
Researchers discovered that Myc's primary function is to repress well-being genes, making cancer cells vulnerable to cell death. This finding suggests a new approach for cancer therapies, targeting the downregulation of well-being genes to enhance the killer activity of Myc in tumor cells.
Scientists at MIT created a new cancer therapy that activates both the innate and adaptive immune systems to attack tumors. The treatment combines an antibody drug with IL-2, which boosts immune responses, resulting in complete tumor disappearance in 80-90% of mice.
Researchers discovered that cancerous tumor cells in soft-shell clams are contagious and can spread from one animal to another. The study found that the cancer originated from a single lineage of tumor cells and has persisted ever since.
Researchers at Cold Spring Harbor Laboratory have discovered that tumor cells can form tubular networks resembling blood vessels, facilitating metastasis in breast cancer. This phenomenon, known as vascular mimicry, allows tumor cells to access the bloodstream and colonize new sites.
Researchers at MIT and Whitehead Institute discover that glioblastoma cells rely on enzyme GLDC to break down glycine, which can be exploited to kill cancer cells. Blocking GLDC activity could offer a new approach to combating brain tumors.
A new review emphasizes the need to decipher immune response dynamics to enhance cancer immunotherapy. Researchers suggest developing combination therapies and biomarker panels to increase treatment impact, as single biomarkers are unlikely to predict patient responses.
Researchers have designed a drug called MP-MUS that targets the energy source of brain tumor cells, crippling their ability to grow and divide. In animal models and human tissue cultures, MP-MUS destroyed 90-95% of malignant glioma cells without affecting healthy brain cells.
Cancer cells with high stress granule levels are more likely to metastasize. Removing YB-1 reduces stress granule formation and decreases metastatic spread in animal models.
Researchers discovered how NORE1A prevents excessive cell proliferation associated with cancer. Overexpressing NORE1A induced cell senescence, whereas removing the protein enhanced cancer-promoting Ras mutations. This study highlights the critical role of NORE1A in regulating tumor growth.
A study published in Veterinary and Comparative Oncology reveals an association between frizzled-6 protein expression and more aggressive behavior in canine bone cancer. The findings may provide a new pathway for tumor formation and improve outcomes for dogs with the disease.
Researchers at Mayo Clinic and the University of Oslo have identified a molecule that transforms normal pancreatic cells into duct-like structures, which can become cancerous. Inhibiting this gene, PKD1, may halt progression and spread of pancreatic cancer.
A new test, PLA test, evaluates the effectiveness of cancer vaccines by detecting tumor antigens presented on MHC molecules. The test has shown promising results in identifying glioma tumors and melanoma cells with specific antigens.
Researchers are developing an irreversible electroporation technique to target and destroy therapy-resistant cells in glioblastoma. The treatment has shown success in animal trials and is now being tested on human cells.
Chronic inflammatory conditions are directly associated with several types of cancer, but the cellular mechanisms behind this link were unclear. An international team of scientists has identified a multistep process showing how these cancers develop, providing potential therapeutic targets for halting tumor cell formation.
Researchers employed a 'Big Bang' model to trace the origins of colorectal cancer cells, revealing clues to why tumor cells become good or bad and potential ways to stop them before they start growing. The study highlights the importance of understanding the early stages of tumor development to prevent cancer.
Researchers at Griffith University have discovered that mitochondria can transfer genetic material between healthy and cancerous cells, leading to rapid proliferation of tumour cells. This finding has implications for our understanding of human biology and may shed light on other diseases with defective mitochondrial DNA.
Researchers found that collagen cross-links play a crucial role in regulating stromal stiffness and determining tumor cell metastatic fate. The study identified two types of collagen cross-links, HLCC and LCC, which are associated with different levels of tumor growth and spread.
Researchers discovered that cells with low levels of profilin 1 protein in breast tumors have increased capacity to metastasize and invade other tissues. The protein regulates the formation of invasive structures called invadopodia, which play a critical role in tumor invasion and metastasis.
Researchers discovered that gene NR2F1 induces dormancy in tumor cells when activated, preventing rapid growth and division. Combining azacytidine and retinoic acid significantly increased NR2F1 activity, leading to improved therapeutic outcomes.