Articles tagged with Cancer Cells
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A Virginia Tech research group has created molecular assemblies that can absorb therapeutic light and activate complexes attached to DNA, allowing for more precise delivery of cancer-killing drugs. Platinum was added to the structure, ensuring the activation of complexes already attached to the target.
Researchers have discovered that the loss of the p63 gene accelerates aging in mice, leading to hair loss, reduced fitness and body weight, progressive curvature of the spine, and a shortened lifespan. This study suggests that p63 plays a fundamental role in maintaining health and preventing cancer.
Researchers found that combining interferon with irinotecan boosts IRF5 protein levels in colon cancer cells, leading to increased cell death. The combination therapy may limit side effects and make it harder for cancer cells to build resistance.
Mutations in genes NF1, c-RET, SDH, and VHL interfere with apoptosis, allowing cancerous cells to evade developmental cell death. This can lead to increased risk of pheochromocytoma and other pediatric tumors.
A study published in Developmental Cell reveals that connective tissue holding a cancer cell in place degrades, allowing it to spread to other parts of the body. The researchers identified a specific pathway critical for cancer cell activity, which could lead to more effective drug therapies with reduced side effects.
A new study has identified a protein called DOCK180 that senses chemicals inducing cell migration. This finding may lead to treatments halting cancer metastasis and immune disorders like arthritis and asthma by inhibiting inappropriate cell movement.
Researchers at Ohio State University have isolated compounds from broccoli sprouts that inhibit the growth of bladder cancer cells. The study found that isothiocyanates, which are formed during digestion, hindered the growth of bladder cancer cells and showed a strongest effect on the most aggressive form of the disease.
The study found that suppressing SIRT1 increases the ability of cells to divide indefinitely without senescence. This discovery has potential applications in generating normal cells for research and could be used in techniques to produce large numbers of cells.
Researchers found that tumor cells use jagged1 protein to interact with endothelial cells, prompting angiogenesis and tumor growth. This discovery could lead to a two-pronged approach to treat cancer by blocking protein secretion and cell contact.
Researchers found that NIPA levels act as a switch to regulate cell division by degrading cyclin B1 during the 'resting' phase. Blocking NIPA causes premature cell division, leading to unhealthy daughter cells. The study sheds light on the role of SCFNIPA in controlling mitosis.
The Albert Szent-Györgyi Prize is awarded to researchers making notable contributions to cancer prevention, diagnosis, and treatment. The $25,000 cash award promotes public awareness of basic science cancer research and encourages increased investment in cancer research.
A new experimental drug PKC412 has been discovered to combat resistant tumors in GIST patients. The study reveals that KIT's reactivation is a crucial factor in tumor cell resistance, and PKC412 can counteract this process.
Researchers found that cells with damaged DNA trigger a mechanism to signal natural killer cells, which attack and destroy cancerous cells. The immune system's ability to identify cancer cells is crucial in preventing tumor growth.
Researchers at UT Southwestern Medical Center discovered a master switch in cell death, which can help control tumor formation and potentially lead to new cancer treatments. The enzyme Mule destroys a key molecule that regulates apoptosis, allowing for the degradation of proteins that control cell death.
Researchers discovered that griseofulvin inhibits cancer cell growth by affecting mitosis, potentially providing a therapeutic advantage when combined with other treatments. The drug has been used for decades to treat fungal infections and shows mild anti-cancer activity.
Researchers found that Gleevec, a cancer drug, slowed the spread of poxviruses in mice. The study suggests that Gleevec might be useful as a preventative against adverse effects of smallpox vaccine.
Cellular behavior exhibits properties of both solid and fluid states, with researchers finding novel nanotechnologies that reveal the fundamental physical laws governing cell mechanics. This discovery offers a new perspective on mechanisms of disease, including airway narrowing in asthma and vessel narrowing in vascular disease.
The Duke team successfully engineered new blood vessels from vascular cells of four elderly men with heart disease, extending their lifespan indefinitely. The treated smooth muscle cells were then impregnated into a biodegradable polymer tube and grew for up to seven weeks, forming functional-like arteries.
Researchers have identified ERG as the first proto-oncogene commonly overexpressed in early-phase prostate cancer, providing a promising target for diagnosis and treatment. The study also found correlations between ERG expression and PSA recurrence-free survival of prostate cancer patients after radical prostatectomy.
Researchers at Johns Hopkins Medicine discovered that the Myc protein controls the production of six microRNAs in human lymphoma cells, which can either promote or slow cell growth. The study's findings suggest a complex system involving Myc, microRNAs, and genes controlling cell proliferation.
Research reveals that mitochondrial activity produces reactive oxygen species that signal low oxygen levels, allowing cells to adapt and respond. Cells with disabled mitochondria fail to detect changes in oxygen availability, highlighting the critical role of mitochondria in oxygen sensing.
Gold nanoparticles have shown to detect cancer cells with 600% greater affinity, using a technique that doesn't require expensive equipment or lasers. The method uses an antibody bound to the particles to target cancer cells, allowing for instant detection and non-toxic results.
Researchers have discovered a novel combination of Velcade and tubacin that is more than twice as effective in killing resistant myeloma cells. This breakthrough could improve patient outcomes by overcoming resistance to existing treatments.
The study reveals the first complete look at the structure of SUMO-1 and its conjugation to other molecules within the complex. Understanding this process could lead to novel anticancer therapies by targeting sumoylation, which promotes cell division.
Researchers are exploring marine natural products as a source of new medicines, including compounds that target cancer cells and regulate calcium flow. One compound, phorboxazole, has shown potential in inhibiting tumor cell growth at low concentrations.
Researchers at Georgia Institute of Technology and University of California, San Francisco discovered that gold nanoparticles can bind to cancer cells using an antibody, making detection easier. The technique has a 600% greater affinity for cancer cells than noncancerous cells and doesn't require expensive microscopes or lasers.
A recent study by Penn researchers found that a metabolic enzyme works with the tumor-suppressor protein p53 to control cellular replication. The enzyme, AMP-activated protein kinase (AMPK), acts as a sensor to detect energy levels in cells and prevents them from replicating under certain conditions.
Researchers found that motexafin gadolinium creates oxidative stress in tumor cells, increasing metallothionein production and inhibiting thioredoxin reductase. This leads to cell death via disruption of critical enzymes needed for cell survival and replication.
Researchers develop customized antibodies that work together to target and destroy cancer cells. The therapy shows significant synergy, with a single combination of antibodies leading to more than three times greater effectiveness than a solo antibody in inhibiting HER2 signaling.
Researchers at the Weizmann Institute have developed a new technology that uses allicin to target and destroy cancer cells. By attaching the enzyme alliinase to an antibody already in clinical use, they can deliver a continuous supply of allicin to penetrate and kill cancer cells.
A clinical trial conducted by Italian scientists found that green tea catechins inhibited cancer cell growth in men with high-grade prostatic intraepithelial neoplasia, leading to a 90% efficacy rate in preventing prostate cancer. The study identified Clusterin as a key mediator of the catechins' action.
Researchers found that selenium metabolite methylseleninic acid (MSA) enhances TRAIL-induced apoptosis in prostate cancer cells, providing a potential novel therapeutic strategy. The study suggests that the combination of TRAIL and MSA may be effective in targeting apoptosis-resistant forms of prostate cancer.
Research reveals that the compound damages DNA by targeting two enzymes: thymidylate synthase and topoisomerase. This understanding could enable combination therapies for greater effectiveness and better patient outcomes. The compound has been shown to be 300-400 times more effective than fluorouracil at killing cancer cells.
Researchers at the Weizmann Institute of Science have determined the structure of a protein complex on retroviruses that enables them to infect cells. The complex undergoes a radical change in shape as it attaches to cells, and its arrangement is unlike other known viral envelope protein structures.
Researchers at The Wistar Institute found that an initiating genetic error can lead to relentless cell division, causing DNA replication stress and breaks. This stress creates conditions for tumor progression and the accumulation of mutant genes, ultimately leading to cancer.
Scientists discovered the ESCO2 gene responsible for pseudothalidomide syndrome through advanced genetic analysis and comparative genomics. The study provides new insights into craniofacial and limb development, health, and disease.
Cantley's discovery of the PI3K signaling pathway has helped explain how normal cells turn into cancerous cells, providing a key target for future cancer treatments. His work has progressed from identifying an unusual lipid kinase activity to uncovering its central role in controlling cancer cell growth and survival.
Research suggests that individuals with more inhibitory killer cell immunoglobulin-like receptors (KIRs) have a decreased risk of developing cervical cancer. Activation of NK cells is thought to contribute to cancer progression by increasing local inflammation, which has been linked to the development of other types of cancer.
Cantley's discovery of phosphoinositide 3-kinase (PI3K) revealed a new lipid produced only when cells are stimulated with growth factors or made cancerous. His work has supported the model that PI3K plays a critical role in many human cancers, and its inhibition is being explored for various diseases.
Researchers develop Fluorform-Assisted Light Inactivation technology to identify proteins involved in cancer cell spread, targeting HSP90A and CD155 molecules.
Researchers from U of T mapped the role of Epstein-Barr virus in cancer, finding that EBNA1 protein disrupts natural cell growth regulation by binding to USP7, increasing cancer risk. This study provides a structural explanation for how EBNA1 impacts cell growth, paving the way for developing better methods to combat viruses like EBV.
Researchers discovered specific phytochemicals in grapes that work synergistically against human DNA topoisomerase II, a key enzyme in cancer cell proliferation. The findings support the argument for eating whole foods and may lead to the development of new anti-cancer strategies.
Researchers discovered a universal cellular mechanism that helps cells release excess water, shedding light on kidney function and potential applications to type 1 diabetes and cancer. This finding highlights the importance of vesicle insertion and phosphorylation in regulating cellular transport.
Researchers developed a new approach to improve cancer treatment by combining DNA-damaging agents with RAD001, a sensitizing agent that targets the p53 protein. This combination could dramatically enhance treatment for solid tumors containing the p53 protein, addressing a long-standing challenge in chemotherapy.
UCSF scientists Joseph DeRisi and Kevan Shokat have made significant contributions to understanding infectious diseases like SARS and malaria, and are now working to develop new treatments. Their research focuses on protein kinases, which play a crucial role in cell signaling and disease development.
The TEL2 gene cooperates with MYC to increase the risk of precancerous B lymphocytes becoming cancerous. This cooperation leads to a mutation inactivating p53, allowing abnormal cells to multiply uncontrollably. The study suggests that TEL2 should be considered a diagnostic marker and/or a target for novel drugs to treat B-cell lymphoma.
Collagen VII protein fragment essential for skin cancer cells to break free and spread, Stanford researchers discover. This breakthrough offers hope for pre-emptive treatment of skin cancers in high-risk patients.
Researchers at Mayo Clinic discovered a new pathway against pancreatic cancer by targeting the GSK-3 Beta molecule, which regulates NF Kappa B activity. This finding may lead to new drug development strategies for other cancers and improve treatment options for pancreatic cancer patients.
Researchers at Duke University have identified specific DNA regions in yeast that are prone to breakage, mimicking cancer cells' chromosomal instability. By slowing down DNA replication, they found that certain retrotransposon sites become more susceptible to kink formation and rearrangements.
Researchers have solved the structure of an essential RNA domain in telomerase, a crucial enzyme in cancer cell division. The discovery provides insights into how telomerase works and could lead to targeted drug interventions.
A new study found that cholesterol plays a crucial role in regulating cell signals by interacting with the oxysterol binding protein (OSBP), which controls the deactivation of ERK. This mechanism helps maintain proper levels of active ERK, preventing cancer growth.
Hexaminolevulinate, a fluorescence-inducing compound, enables early detection of superficial bladder cancer lesions. This increases the five-year survival rate to 90% and reduces recurrence rates.
Researchers found celecoxib reduces prostate cancer cell growth and proliferation by targeting both COX-2 and cyclin D1. In animal models, celecoxib also reduced tumor mass and blood vessel density, suggesting a potential new therapeutic approach for treating prostate cancer.
A Yale research group found that CTCL cells require antigenic stimuli delivered by Langerhans cells to replicate. The study identified cryptic self-antigens presented by LC to CTCL receptors, stimulating rapid division and regulatory T cell formation.
The study shows that blocking CK2 activity makes cancer cells sensitive to TRAIL-induced apoptosis, a promising strategy for treating colorectal cancer and other solid tumors. Researchers used a CK2-inhibitor or short hairpin RNA to block CK2 activity, sensitizing cancer cells to TRAIL and inducing cell death.
Researchers at Dana-Farber Cancer Institute have developed a new compound, AMN107, which targets Bcr-Abl kinase protein responsible for CML growth. In laboratory cell cultures and mice with the disease, AMN107 demonstrated effectiveness in killing CML cells and inducing longer remissions compared to Gleevec.
A UCLA study found that green tea extract may help fight bladder cancer by interrupting the development of invasive cells. The extract affects actin remodeling, a process crucial for cell movement and invasion.
A mouse model of leukemia reveals a causal link between Shp2 mutations and leukemia, pointing to these mutants as attractive therapeutic targets. The study's findings suggest that current treatments are often ineffective and highlight the need for clinical trials of Ras/Mek inhibitors.
A novel sensor has been developed to measure tiny changes in cell volume, providing real-time results for antibiotic sensitivity testing. The technology, known as 'cell volume cytometry,' is highly sensitive and can detect changes in cell dimensions never seen before in living cells.
Researchers using 'heavy water' tracked leukemia cell birth and death rates, revealing dynamic process with mortal cells that proliferate and die. The study found faster birth rates of leukemia cells correlate with poorer patient outcomes, paving the way for potential new methods of prediction and treatment guidance.