Articles tagged with Tumor Cells
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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.
Scientists have identified CD161 as a potential new target for immunotherapy of malignant brain tumors, including glioblastoma. The molecule suppresses the cancer-fighting activity of immune T cells, but blocking its pathway enhances the killing of tumor cells and improves survival rates in animal models.
This review article highlights the complex crosstalk between cancer stem cells (CSCs) and tumor-associated macrophages (TAMs), two key players in cancer progression. CSCs have been identified as the drivers of cancer initiation and progression, while TAMs create a protective microenvironment for CSC development and dissemination.
Researchers found that non-metastatic cells can spread to distant organs through a new mechanism involving the fibrotic niche induced by malignant cells. This discovery suggests targeting the fibrotic niche as a promising strategy to control solid tumor progression.
Researchers discovered that immunomodulatory drugs like lenalidomide and pomalidomide starve cancer cells by destabilizing essential surface proteins, ultimately inhibiting tumor growth. This finding opens up new possibilities for targeted therapies in multiple myeloma.
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.
Researchers have identified a little-known glycoprotein called stanniocalcin-1 that blocks the immune system's ability to fight cancer cells. By targeting this pathway, scientists hope to improve response rates to cancer immunotherapy treatments.
Researchers at MIT have devised a way to label and sequence individual RNA molecules within a tissue sample, allowing for a unique snapshot of which genes are being expressed in different parts of a cell. This technique offers new insights into how gene expression is influenced by a cell's location or its interactions with nearby cells.
Researchers at Tokyo University of Science explore the structure of porphyrin derivatives to selectively target cancer cells and improve drug delivery. They found that meso-derivatives accumulate in cells at 3-fold higher amounts than β-derivatives, and that smaller functional groups allow better aggregation.
Researchers at Boston University School of Medicine have identified genetic dependencies in tumors that have undergone whole genome doubling. The study found that WGD tumor cells possess unique vulnerabilities that can be targeted by new therapeutics.
Researchers developed a BCL strategy to generate highly potent tumor-targeted drugs from non-toxic compounds within the tumor, avoiding decomposition and side effects. The targeting drug Ru-rhein exhibits high anti-cancer activity against lung cancer cells while being non-toxic to normal cells.
Researchers at UT Southwestern Medical Center have discovered that removing a key gene called Cbl-b can revitalize exhausted CD8+ T cells to combat malignant tumors. This breakthrough could offer a new approach to harnessing the body's immune system to fight cancers.
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.
Cancer cells can thrive in hostile environments through metabolic adaptation known as the Warburg Effect. Moffitt researchers found that activation of transcription factor KLF4 allows cells to select for this phenotype, enabling them to survive and thrive in poor conditions.
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 developed CopyKAT, a new computational technique that accurately differentiates between cancer and normal cells in solid tumor samples. The tool uses gene expression data to identify aneuploidy and distinct subpopulations within cancer cells.
A new study published in Cell reveals that RNA splicing therapeutics can activate antiviral immune pathways in triple negative breast cancers, triggering tumor cell death and signaling the body's immune response. The discovery highlights a novel mechanism for turning on the immune system in aggressive cancers.
Researchers developed a gene expression signature that robustly predicts patient survival in patients with peritoneal carcinomatosis, a form of metastatic gastric cancer. The signature is associated with tumor cell populations and lineage compositions, offering potential for tailored treatment strategies.
Researchers have developed molecular reporters that reveal how immune cells strengthen brain tumors, making them more aggressive. The technology has the potential to guide therapy development and is applicable to various biological systems.
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.
Researchers found that targeting the fas protein can prevent cancer cells from escaping immunotherapies, leading to longer-lasting positive responses and improved survival rates. By combining immunotherapies with small molecule inhibitors, bystander tumor cell killing may be potentiated to eliminate antigen-loss variants.
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.
Research suggests stress hormones and immune cells may contribute to tumor recurrence by reactivating dormant cancer cells. Targeting stress hormones with approved drugs like beta-blockers could potentially prevent tumors from returning.
Researchers at Brigham and Women's Hospital developed a small-molecule inhibitor targeting SerpinB9 protein in cancer cells, weakening its defense mechanisms and triggering cell death. The approach shows promise for treating 'cold tumors' that evade immunotherapies.
A study by Harvard Medical School scientists reveals a transient, cooperative interaction between ovarian cancer cells that allows nonmetastatic tumor cells to invade distant sites. The team identified amplified ERBB2 levels in a specific cell population, which was activated by amphiregulin, a signaling protein found in advanced ovaria...
The new WEHI-TV animation explains how the 'tumour suppressor' protein p53 prevents cancer-causing changes in cells. More than half of human cancers involve faulty p53, and researchers are still working to develop better therapies for these cancers.
Researchers have identified a gene, VSIG1, that prevents the development of metastatic tumour cells, enabling targeted therapies to be developed. The study validates the use of spiked-scRNAseq technology for testing drugs against metastases, including personalized approaches.
Researchers from Tokyo Medical and Dental University identify TruB1 as a regulator of the microRNA let-7, which has significant implications for cancer development and suppression. The study reveals that TruB1 promotes maturation of let-7 and suppresses cell growth and division.
Pancreatic cancer cells use nerve growth factor to signal nerves to grow into dense tumors and secrete nutrients like serine. This allows the cancer cells to multiply despite nutrient starvation, highlighting a unique adaptation that contributes to their deadliness.
This study examines the effects of talc on mesothelial and neoplastic cells, revealing high levels of IL-6 and TNFRI. The results suggest that normal mesothelium is the main stimulus for the inflammatory process, with talc inducing higher rates of apoptosis in neoplastic cells.
Researchers at Swiss Federal Institute of Technology and Philochem AG describe four novel formats for L19-IL2 fusion proteins, featuring different arrangements of antibody and IL2, which exhibit superior tumor-targeting properties in vivo. The new format also reduces activation of regulatory T cells.
A new technique developed at Scripps Research isolates tumor-reactive immune cells in just one day, offering a platform for personalized cancer treatments. The method, called FucoID, detects and tags the surface of sought-after immune cells using an enzyme, enabling their detection with fluorescent probes.
A new study by Brown University scientists has identified vimentin as a potential target for treating aggressive cancer cells known as polyploidal giant cancer cells (PGCCs). PGCCs have been found to rely on vimentin to migrate and invade surrounding tissues.
Researchers have discovered that cancer cells use their nucleus to sense environmental compression and trigger responses to evade overcrowded areas. The study proposes a new mechanism by which tumor cells cope with the lack of space and compressive stresses, involving the unfolded and stretched nuclear membranes.
Researchers developed nanoparticles that release bursts of calcium inside tumor cells, inhibiting drug pumps and reversing MDR. The treatment showed significantly smaller tumors in tumor-bearing mice with no apparent side effects.
Researchers define two molecular subtypes of pancreatic carcinoma with distinct aggressiveness, differing in the origin and development. The study reveals a novel mechanism called viral mimicry that promotes cancer growth and metastasis.
Scientists from Germany and China combine chemotherapeutic and photodynamic agents in a nanocapsule to destroy cancer cells. The treatment is effective against resistant tumors and stops tumor growth in live mice, offering a promising new approach to cancer therapy.
Researchers discovered that immune system T cells can home-in on tumor cells independently of intermediary immune cells and release chemical signals that attract more T cells. This 'swarming' behavior could help develop new cancer therapies targeting solid tumors, currently less responsive to immunotherapies.
Researchers from RUDN University have developed a novel domino reaction for synthesizing chromenoisoquinolineamine derivatives, which showed promising antitumor activity against cancer cells, including drug-resistant strains. The new compounds were found to be toxic to tumor cells and efficient even at low concentrations.
This study reveals that hypoxic exosomes promote sphere formation and stem-like phenotype in EWS cells by delivering enriched miR-210. The knockdown of HIF-1α led to decreased exosomal miR-210 levels, while inhibition of miR-210 attenuated sphere formation.
Researchers at CNIO successfully applied CRISPR technology to eliminate fusion genes causing tumors, leading to the death of cancer cells while leaving healthy cells unaffected. This breakthrough approach could lead to the development of targeted cancer therapies.
A new potential drug treatment has been discovered for a type of lung-cancer. Researchers have found that combining osimertinib with linsitinib can cure or delay tumor recurrence in EGFR-mutated lung cancer, even in AXL-low expressing tumors.
Researchers discover that the proteins transforming growth factor-β (TGF-β) and tumor necrosis factor alpha (TNF-α) promote the development of cancer-associated fibroblasts, contributing to tumor progression. TGF-β induces endothelial-mesenchymal transition (EndMT), a process involving the conversion of endothelial cells to CAFs.
Researchers used single-cell sequencing to genetically identify cell types and subtypes in pancreatic tumors and surrounding stroma. The study identified distinct cell populations, including tumor cells, immune cells, and cancer-associated fibroblasts, which correlated with patient clinical outcomes.
Researchers at University of Würzburg developed a drug that can disarm Aurora-A kinase, a protein that causes extensive damage in cancers like leukemias and neuroblastomas. The new PROTAC substance completely degrades the Aurora protein in cancer cells, leading to cell death.
Researchers at the Complutense University of Madrid found that childhood leukemia tumor cells hide in the choroid plexus of the brain, allowing them to escape chemotherapy and cause relapses. This discovery could lead to more effective treatment strategies to prevent these cells from colonizing the CNS.
Researchers found that Brat tumors in Drosophila are highly oxidative, with increased oxygen consumption rates compared to normal brains. Oxidative metabolism plays a key role in tumor cell immortalization, driven by mitochondrial fusion and increased efficiency in oxidative phosphorylation.
A new study found that tumor cells outcompete T cells for the amino acid methionine, impairing its function. Supplementing methionine can restore T cell function, suggesting a potential target for immunotherapy against more cancers.
Scientists have identified a promising new system to attack tumors directly by combining a small biomolecule with a toxic metal complex. The molecule's luminescent properties allow for detection within cells and demonstrate its toxic effect, paving the way for further research into this innovative theranostic system.
Researchers found that EMT promotes successful rounding and cell division in tumor cells, making them stiffer while surrounding non-dividing cells become softer. The study suggests a new direction for understanding how EMT influences cancer cell behavior.
Breast cancer cells can exist in different cellular states, ranging from stem-like cells to more differentiated cells. Researchers identified a complex spectrum of cell states between different tumor types, which can range from stem-cells to 'beginner cells' and more differentiated cells.
Research found that cancer cells losing 'stickiness' allows them to move freely, but dense environments can still hold them back. This contradicts previous understanding of cell movement in cancer development.
Scientists create genetically engineered, off-the-shelf therapeutic T cells that can recognize and kill specific cancer cells without requiring personalized training. The 'off-the-shelf' approach solves limitations of original cell immunotherapy methods by avoiding time-consuming processes and resulting in more potent cells.
A study found that younger and female patients accumulate more cancer-causing genetic mutations, making them less visible to the immune system. This selective pressure leads to poorer response rates to immunotherapy.
Breast cancer cells send pro-tumorigenic messages to normal cells through extracellular vesicles, reprogramming mitochondrial function and promoting migration. This process may provide a novel target for disrupting cancer progression.
Scientists discovered that identifying tumor-associated macrophage patterns in lung tumor tissue enables the prediction of disease progression. The study found that a higher number of tumor-promoting macrophages near the invasive margin is associated with lower patient survival rates.
Cancer cells release small vesicles called exosomes that can re-programme surrounding cells, driving tumour growth and metastasis. The newly discovered Rab11a-exosomes may help cancers evade treatments.
Tiny finger-like projections called filopodia play a crucial role in invasive behavior of rare lung cancer cells. The cells have longer filopodia than their counterparts, which is linked to the gene MYO10, stabilizing these structures. This discovery could help develop treatments that prevent cancer from spreading.
Cancer researchers identified a previously unseen cell state that enables tumors to develop resistance to chemotherapy, and found this adaptable cell type in every tumor they examined. This discovery offers hope for developing targeted therapies to combat cancer's adaptability and provide longer-lasting remissions.
Researchers at MIT and Harvard University have mapped out an additional layer of control guiding tumor evolution through epigenomic alterations. They identified 11 chromatin states that cancer cells can pass through as they become more aggressive, and found a key molecule linked to advanced lung cancer forms.