Articles tagged with Cancer Cells
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Scientists have identified a protein that regulates cancer cell spread and normal tissue cell shedding, potentially leading to new treatments. The research suggests that metastasis is not an abnormal process limited to cancer but a normal process used by healthy cells.
A study published in Science reveals that tumor cells with a specific mutation release a chemical metabolite that weakens nearby immune cells, rendering them less capable of killing cancer cells. The findings highlight the critical role of the tumor microenvironment in cancer growth and provide insights into developing targeted therapi...
Researchers developed a computational platform to identify metabolic vulnerabilities in ovarian cancer genes, suggesting opportunities for targeted therapies. The study found that certain genetic alterations can create vulnerabilities in cancer cell metabolism, which can be exploited to selectively kill cancer cells.
Researchers at the University of Helsinki have identified target genes of the MYC oncogene responsible for its growth-promoting effects. By modifying these genomic binding sites, they slowed down cell growth. This finding has significant implications for developing new cancer treatments.
Scientists successfully inhibited cancer cell growth using a modified pyrrolizidine alkaloid that avoids liver damage. The approach uses 'on-site synthesis' near cancer cells to limit toxicity.
Researchers at UEA discovered that 'normal' prostate cells in men with prostate cancer have specific genetic changes that facilitate the growth and spread of cancer. The study suggests treating the whole prostate, not just affected areas, may be more effective.
A team of researchers has identified TSG101 as a crucial regulator of the PARP1 enzyme, which is responsible for repairing DNA damage. In cancer cells with BRCA mutations, TSG101 is essential for PARP1 activation, making it a promising target for cancer treatment.
Tel Aviv University researchers discovered that skin cancer cells interact with astrocytes in the brain, promoting metastasis. By inhibiting this interaction using existing treatments, they delayed the spread of melanoma to the brain by 60-80%. This breakthrough has implications for treating advanced-stage melanoma.
Researchers at German Cancer Research Center have found that persulfides, small molecules produced by cells, efficiently suppress membrane damage and ferroptosis. Persulfides act as radical scavengers, interrupting the destructive chain reaction threatening cell integrity.
Researchers discovered that autophagy facilitates the elimination of cancer cells via cell competition, highlighting its potential as a target for cancer prevention and treatment. The study sheds light on the role of autophagy in maintaining tissue homeostasis and opening avenues for novel anti-cancer therapeutics.
A new intracellular checkpoint gene, CISH, has been found to suppress the ability of human T-cells to recognize and attack cancer cells. When CISH is disabled, T-cells more effectively recognize mutated proteins produced by tumors, making them more responsive to existing checkpoint therapies.
Researchers at University of California - San Francisco have developed a new therapy that overcomes cancer cell barriers and marks them for destruction by the immune system. By pulling mutated KRAS protein to the surface, the drug acts as an “eat me” flag, allowing immunotherapy to eliminate all cells bearing this flag.
Bladder cancer researchers discovered a subset of CD8 T cells that adapts to tumor evasion strategies, offering a strategy to reduce tumor cells' ability to fight them off. The study also identified potential ways to make immunotherapy more effective against this deadly cancer by targeting the HLA-E/NKG2A axis.
A study led by University of Pennsylvania scientists reveals how tumor-derived factors stimulate trogocytosis, a process that can help cancer cells evade detection and grow unchecked. Blocking this process improved the effectiveness of CAR T cell therapy in mice.
Researchers have developed a new safety system for CAR-T cells, called VIPER CAR-T cells, that can be turned on or off. This allows doctors to target cancer more aggressively while minimizing side effects. The new system uses an FDA-approved antiviral drug to control the cell's activity.
Researchers have developed a synthetic drug that stops cancer cells from producing energy by blocking oxygen conversion. The tiny hairs formed by the drug's molecules can kill even aggressive and untreatable cancer cells within four hours.
The PROSPER RCC trial showed no difference in recurrence-free survival between arms, with higher adverse events reported in the nivolumab arm. The trial's results inform future research on neoadjuvant trials in high-risk renal cell carcinoma.
A new imaging technique called LC-OCT significantly improved the accuracy of basal cell carcinoma (BCC) diagnosis by 12% compared to clinical and dermoscopic examinations. The technique provided detailed 3D images at a cellular level, enabling more accurate differentiation between BCCs and other skin conditions.
Scientists identified a key event in persister cell survival, finding that cytochrome c release kickstarts the integrated stress response pathway, promoting gene expression that prolongs survival. This process may lead to cancer recurrence and resistance to other treatments.
Researchers discovered that combining a new target with an old chemotherapy drug can reduce resistance and potentially improve treatment outcomes for small cell lung cancer. The study used mouse models to show that inhibiting a protein called SMYD3, along with cyclophosphamide, stopped tumors in their tracks.
Researchers have identified fascin as a key player in promoting cancer development, with the protein controlling cell movement and invasion. Forcing fascin into the nucleus of cancer cells could prevent their growth and movement.
A combination of immunotherapy and virotherapy using myxoma virus provides new hope for patients with treatment resistant cancers. The approach boosts the immune capacity to effectively target and destroy cancer cells, inducing a form of cell death called autosis.
A KAUST-led research team identified two drug treatments that boost the activity of molecules involved in cell adhesion, enhancing the ability of blood-forming stem cells to enter the bloodstream and produce new blood. This breakthrough could lead to improved bone marrow transplant success for leukemia patients.
A University of Houston engineer has developed technology to determine which patients are likely to respond to CAR T-cell therapy for lymphoma, saving time and increasing success rates. The TIMING method analyzes interactions between T cells and tumor cells, identifying a key ligand molecule that predicts patient response.
Australian researchers have discovered a new mechanism by which T cells can react to lower doses of antigens, leading to a 50-fold increase in T cell activation sensitivity. This finding opens up new possibilities for developing more effective immunotherapies.
EdU, a common DNA labeling molecule, triggers a runaway DNA repair process that is fatal to cancer cells, including those in the brain. This discovery opens up new possibilities for using EdU as an anticancer agent, particularly for fast-dividing cancerous brain cells.
The discovery reveals that the nucleus deforms like a liquid drop, preserving its shape and protecting its genome. This understanding may lead to new approaches for treating cancer by aiding cell nuclei in regaining their normal shapes.
A new study from the University of Alabama at Birmingham reveals how impaired metabolism due to mutations in succinate dehydrogenase B disables a normal bioenergetic sensing mechanism, leading to uncontrolled cell proliferation. This discovery sheds light on how cancer cells divide despite having a less efficient energy production.
Researchers at Washington University in St. Louis found that cancer cells metabolize glucose in their mitochondria, following conventional biochemical patterns. The study suggests that limiting glucose uptake may not be an effective strategy to target cancer cells, and glucose metabolism may need to be reevaluated as a therapeutic target.
Researchers at Kyoto University have developed a cancer therapy model that utilizes a protein degrading system to transiently degrade and reduce the PD-1 protein, which blocks immune function. This approach has shown high therapeutic efficacy in inhibiting cancer cell growth in mice.
Researchers at IRB Barcelona have found that CRISPR/Cas9 gene editing can trigger cell toxicity and genomic instability, particularly in regions near the tumour suppressor protein p53. The study identified 3,300 targeted spots with strong toxic effects, highlighting the need for safer CRISPR reagents.
ARID1A-deficient bladder cancers are sensitive to combination therapies with the EZH2 inhibitor GSK-126 and inhibitors of PI3K, acting synergistically. The research found that tumors deficient in ARID1A protein have elevated levels of PIK3R3 and phosphoAKT.
Researchers developed a monoclonal antibody that binds E-cadherin, strengthening cell adhesion and preventing cancer metastasis. The antibody, 19A11, has two binding modes that increase adhesive strength through salt bridge formation.
A new sample preparation method called 'water droplet-in-oil' (WinO) has been developed to improve efficiency in single-cell proteomics. The technique reduces sample loss and increases throughput by up to 10-fold compared to conventional methods.
Researchers at the Centre for Genomic Regulation have identified PDIA6 as a key protein involved in driving melanoma malignancy. The study found that PDIA6 promotes melanoma cell growth by binding to RNA molecules inside tumor cells, making it a promising therapeutic target.
SLFN11 acts as a surveillance factor for protein homeostasis by alleviating proteotoxic stress derived from protein synthesis and maturation. Its lack makes cells vulnerable to anticancer drugs inducing ER and proteotoxic stress, leading to chemoresistance. SLFN11 is also involved in regulating immune response and inflammation.
A new study by Tokyo University of Science researchers reveals that dendritic cell immunoreceptor (DCIR) plays a crucial role in the development of colorectal tumors. Blocking DCIR may prevent ulcerative colitis and colon cancer, offering a potential therapeutic target for treating these diseases.
University of Cincinnati researchers have discovered a technique using light-activated proteins to normalize dysfunctional mitochondria in cells. This method has the potential to treat certain diseases, including cancer and neurodegenerative disorders.
Leukemia cells exploit metabolic pathways to evade programmed cell death, but researchers identified a weak spot in acute lymphoblastic leukemia that can be targeted with experimental drugs. Inhibiting glutathione metabolism induces ferroptosis, leading to the death of malignant lymphocytes.
Researchers created a novel tumor organoid system to examine the impact of bacterial metabolites on immune checkpoint blockage, a promising cancer treatment. The system showed that certain bacterial-released factors improved immune cell viability and increased treatment efficacy.
Researchers discover gene AVIL responsible for deadly brain tumor also causes two forms of childhood cancer, rhabdomyosarcoma. Blocking AVIL activity prevents formation of the disease in lab samples and mouse models.
Researchers used Guardant NGS to analyze nearly 17,000 lung cancer samples and found MET amplification in 1.2% of cases, with 20.8% having overlapping oncogenic drivers. The study suggests that high gene copy numbers and smaller amplified regions can be used to enrich for the true MET-sensitive population.
A study published in Nature Physics reveals that specialized cell movement may explain the progression of cancer and cystic fibrosis. Cells with ruffled edges sense viscosity and adapt to increase their speed, moving faster through mucus than blood. This discovery sheds light on disease mechanisms and potential treatments.
A new study from Tel Aviv University found that CRISPR therapeutics can lead to a significant loss of genetic material in treated cells, potentially destabilizing the genome and promoting cancer. The researchers detected up to 10% of cells with lost chromosomes, highlighting the need for extra care when using this technology.
A new study from MIT and Broad Institute researchers analyzed interactions between nanoparticles and nearly 500 types of cancer cells, revealing thousands of biological traits that influence cell response. The findings could help tailor drug-delivery particles to specific types of cancer.
Researchers discovered cancer cells produce a unique collagen that alters the tumor microbiome and promotes cancer progression. Loss of this collagen reduces cancer cell proliferation and boosts anti-tumor immune response, offering a potential therapeutic strategy.
Researchers developed a new blood test that analyzes circulating tumour DNA, providing unprecedented insight into cancer make-up. The test reveals unique characteristics of each patient's cancer, enabling personalized treatment plans. It also sheds light on treatment resistance and helps predict effective treatments.
Scientists from A*STAR and NUS Cancer Science Institute identified a key cancer progression mechanism that could lead to more effective treatments. The discovery involves reactivating the hTERT gene, which is responsible for prolonging telomeres in cancer cells.
Scientists use a unique tool to apply mechanical forces that affect protein folding, revealing talin's interaction with tumor-suppressing protein DCL1. This discovery provides insight into the antitumor effect of DCL1 and potential new treatments for metastatic cancer.
Researchers at Edith Cowan University have found a genetic link between human leukocyte antigens and immunotherapy side effects in non-small cell lung cancer patients. The discovery enables doctors to tailor treatment to individual patients, reducing the risk of toxicities and improving overall outcomes.
The Mount Sinai Hospital has been awarded $4.2 million over five years to establish a Proteogenomic Data Analysis Center, which will help identify potential biomarkers and drug targets for cancer and new insights into cancer biology.
Researchers from Tokyo University of Science developed novel complex-peptide hybrids that induce programmed cell death in apoptosis-resistant cancer cells through paraptosis. The compounds, syn-6 and anti-6, inhibit cell death by uncoupling mitochondrial calcium uptake and inducing cytoplasmic vacuolization, leading to cell death.
A new machine learning model uses network-based biomarkers to predict patient response to immunotherapy in multiple cancer types, enabling personalized treatment plans. The study improves upon conventional methods, increasing accuracy and benefiting more patients.
Researchers have successfully mapped the atomic structure of the nuclear pore complex using X-rays, providing a framework for understanding cell function and developing new therapies. The completed human NPC puzzle will enable future experiments on NPC function and its relationship to diseases.
Researchers at Osaka University identified Src as a key molecule in the process of epithelial cells becoming invasive and cancerous. The study found that CDCP1 forms a molecular scaffold that activates Src, promoting cancer cell invasion.
Researchers have found that high levels of iron can generate toxic free radicals, which damage lipids and ultimately lead to cell death. The team is exploring the use of compounds like JKE-1674 to induce ferroptosis in prostate cancer cells, making them more vulnerable to treatment.
A new atlas of tissue-resident memory T cells reveals their adaptation to distinct tissue environments, offering insights into immune defense strategies. The study's findings could inform the development of targeted vaccines and therapies, leveraging 'first responders' in tissues vulnerable to infection.
Researchers have found a new approach to treat cancer by using plasma treatment, which induces apoptosis in cancer cells without harming normal cells. The equivalent total oxidation potential (ETOP) has been defined as a plasma dose, providing a dose-response relationship for different cell types.
A recent survey revealed significant gaps in cancer screening among women aged 50-64, with rates as low as 50% for colorectal cancer and 46.5% for both cancers. The study found that patient-centered approaches to screening can facilitate timely testing and management of abnormal results.
Researchers found that suppressing an enzyme called MSRA, which fixes oxidative damage to proteins, sparks the metastatic spread of pancreatic cancer cells. The discovery suggests that similar switches may exist in other cancers and lays the groundwork for redox-based targeted therapies.