Articles tagged with Cancer Cells
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Researchers at Ohio State University have made a breakthrough in understanding how cells package DNA, with implications for cancer research and new therapies. A newly discovered protein, Hif1p, works with an enzyme complex to add histone proteins to DNA, forming chromatin.
A study by Johns Hopkins Medicine found that a gene defect, PASG, is linked to premature aging in mice. The researchers discovered that the mutated gene causes cells to age and die prematurely, leading to growth problems and early death.
Researchers found that administering opioid growth factor (OGF) to patients with advanced pancreatic cancer improved their quality of life and survival rates. OGF was shown to be non-toxic and did not cause common side effects associated with chemotherapy, such as hair loss or nausea.
Dr. Xiaodong Wang, a professor of biochemistry at UT Southwestern Medical Center, has been elected to the National Academy of Sciences for his groundbreaking research on cell death and apoptosis. His discoveries could lead to treatments for cancer and neurological diseases.
Prostate cancer cell lines exhibit high levels of free radical damage and defective repair mechanisms, leading to a cascade of events culminating in further DNA damage and cellular dysfunction. The new research provides solid evidence for the critical role of free radicals and repair in prostate cancer development.
Researchers at UIC discovered a gene, Foxm1b, essential for the multiplication of cancer cells. A potential drug was created to block Foxm1b activity, starving tumor cells and preventing their growth.
Researchers analyzed E. coli's chemotaxis system to understand signal transduction networks, a universal design principle in nature. They found that individual variability can be regulated and carried important information about molecular mechanisms.
The U-M group uses lab-made dendrimers as the backbone of their delivery system, which can attach targeting agents to recognize cancer cells and deliver lethal doses while leaving normal cells unharmed. Early results show that nanoparticle drugs effectively treat cancer with fewer side effects than conventional chemotherapy.
Researchers at USC's Viterbi School have developed a new electric pulse technology called electroperturbation, which exposes cells to brief and intense electric pulses that can trigger cell death. The technique has advantages over conventional treatments, being non-invasive and able to deliver treatment remotely.
USC researchers have discovered a unique DNA structure linked to follicular lymphoma, the second-most common form of non-Hodgkin's lymphoma. The fragile site on chromosome 18 is responsible for 4% of all cancers and leads to the translocation 14;18, making cancer cells invincible.
SLC5A8 transporter enables the colon to absorb short-chain fatty acids, produced by bacteria fermenting plant cell walls, for energy. This finding supports eating vegetables to limit antibiotic use and promotes a healthy gut microbiome.
Researchers have discovered that low-dose HDAC inhibitors can prevent the production of inflammatory cytokines, reducing cell damage and improving survival rates in mice with GVHD. The study suggests that these drugs may be used to reduce the risk of death, hospitalization, and serious side effects associated with bone marrow transplants.
A new study by St. Jude/Mayo Clinic researchers found a direct link between the CBP gene and lymphoma development in mice, with the loss of CBP promoting T-cell lymphoma and cooperating with reduced p27Kip1 protein levels. The study suggests that CBP plays a role in cancer development despite normal p53 activity.
The Mayo Clinic's new biofusion technology targets cancer tumor cells by exploiting the natural tendency of fused cells to kill each other. This approach also promotes immune responses and repairs damaged tissues, offering a promising platform for anticancer treatment and vaccine delivery.
Researchers discovered a specialized DNA polymerase that can rescue stalled replication processes when encountering foreign material, even if it contains damage. This shows the remarkable ability of cells to reproduce and cope with genetic errors.
The study found that vinculin changes its shape in response to protein binding, enabling it to regulate cell movement and adhesion. This versatile protein plays a critical role in both healthy development and disease progression, including cancer cell spread.
Scientists have developed a method that uses allicin, found in garlic, to selectively kill cancer cells in mice. The method involves injecting an antibody and enzyme combination that targets specific receptors on cancer cells, triggering the production of lethal allicin molecules that destroy tumors while leaving healthy cells intact.
Researchers found that cancer cells release signals to nearby blood vessels to stimulate new vessel growth, while blood vessels release signals to sustain migrating cancer cells. This two-way dialogue allows cancer cells to survive and grow before new blood vessels form.
H. Steven Wiley and colleagues use systems biology to analyze the EGFR receptor network, revealing surprising complexities. They predict that lower-affinity ligands can bind longer, allowing for more effective cancer treatments.
Researchers have discovered that Heat shock protein (Hsp) 70.1 and 70.3 can be used to increase cancer cells' vulnerability to radiation treatments, offering a new treatment window for cancer patients. The proteins were found to interact with telomerase, an enzyme that helps maintain the telomeres at the ends of chromosomes.
Researchers at the University of Illinois at Urbana-Champaign have identified anastellin, a natural agent derived from the cell adhesion protein fibronectin. Anastellin stabilizes the extracellular matrix, restricting the motion of cancer cells and creating strong 'jail bars' to prevent metastasis.
A new compound has been found to selectively kill cancerous cells while leaving healthy white blood cells intact. The compound, called 13-D, induces apoptosis in cancer cells by activating caspase-3 and causing cell shrinkage, a desirable outcome as it reduces the risk of side effects.
The discovery of protein EB1 at the tip of Chlamydomonas flagella sheds new light on intraflagellar transport (IFT) and its regulation. IFT is crucial for flagellar growth and maintenance, and EB1 may play a key role in controlling the molecular transport system responsible for IFT.
Recent research suggests that at least eight central 'clock' genes coordinate cell proliferation and apoptosis in circadian time. Studies have shown that tumor growth is organized within a daily cycle, with tumors growing twice as fast during the active phase. This discovery may lead to new therapeutic targets for cancer treatment.
Researchers will discuss novel targets for controlling cancer growth, such as the circadian rhythm of cells and VEGF, a key player in tumor angiogenesis. The conference also aims to improve radiotherapy effectiveness for head and neck cancers by tailoring therapy to individual tumors.
Researchers at DMS have found that removing RIP140 allows retinoids to effectively differentiate cancer cells, slowing tumor growth and increasing the efficacy of cancer treatment. This breakthrough sheds light on the potential benefits of retinoid-based therapies for various types of cancer.
Researchers are studying the effects of low doses of radiation on zebrafish embryos to understand DNA damage and repair mechanisms. The study aims to determine the threshold for damage and whether certain genes and proteins can prevent or repair damage, with potential implications for human health.
Researchers at St. Jude Children's Research Hospital have discovered that PUMA is the primary mediator of cell death in response to p53 signals, leading to apoptosis in cancer cells. The study provides critical insights into how cancer disrupts a failsafe mechanism that kills abnormal cells, and offers potential new therapy targets.
Scientists discovered that specific DNA damages cause transcriptional mutagenesis (TM) in non-dividing cells, leading to mutant protein creation. TM can contribute to neurodegenerative diseases, cancer, and aging by causing faulty proteins to be produced during normal cellular processes.
Scientists have discovered that cells can adapt to survive without oxygen, a key finding that could lead to new treatments for cancer, heart attack, and stroke. Researchers are tracing the signaling pathways for cell injury and death, with hopes of identifying therapeutic tools to switch cellular behavior.
Researchers at UCSB have identified a cell survival gene, ICD-1, that prevents normal cells from committing suicide. The discovery may lead to new treatments for degenerative diseases such as ALS, stroke, heart disease, autoimmune disorders, and cancer.
Researchers found that the HIV vpr gene exploits the normal repair process of cells to stop vital white blood cells from replicating, thus disabling the immune system. The study suggests a possible treatment for AIDS-related immune-system damage using medicines that prevent the human ATR gene from being activated by HIV's vpr gene.
Researchers found endostatin treatment reduced invasive head and neck cancer cells by half and their migratory capabilities by one-quarter. The study suggests an implanted drug delivery system could provide sustained therapeutic drug levels directly to tumors.
The consortium aims to identify and measure all lipid types within a cell, improving understanding of their role in diseases. This knowledge will help develop more effective diagnostic devices and treatments for conditions like cardiovascular disease and inflammatory disorders.
Scientists discovered two green tea compounds, EGCG and EGC, that inhibit the aryl hydrocarbon (AH) receptor, a molecule linked to cancer. The findings suggest that green tea may exert its anti-cancer activity through multiple pathways.
A new study has found that a weekly regimen of paclitaxel and carboplatin is well-tolerated and effective in treating advanced non-small cell lung cancer. The treatment resulted in a response rate of 32% and median survival time of 49 weeks, with fewer side effects compared to standard regimens.
Researchers at the University of Pennsylvania identified Pim-2 as a critical enzyme in the survival of cancer cells. The study found that Pim-2 operates independently from the Akt pathway, allowing cancer cells to survive even when starved or deprived of growth factors.
Researchers used RNA interference to impair cancer cells' ability to produce telomerase, resulting in a 85% shortening of telomeres over 75 days. The technique reduces but doesn't fully block telomerase production, paving the way for potential therapy against most cancers.
Studies found that increasing TBP levels can contribute to oncogenesis, while p53 acts as a tumor suppressor by reducing TBP's effective concentration. These findings have implications for the development of new cancer treatments and therapies.
Researchers at Johns Hopkins Medicine found that pancreatic cancer may be triggered by the reactivation of a growth signal normally turned off in adult tissues. By blocking this pathway, they hope to prevent the early cellular changes leading to cancer.
Researchers Jules Berman and Donald Henson developed a classification system for cancer precursors, identifying 568 distinct concepts with over 4700 terms. This database is designed to be fully searchable and linked to other databases, providing a potential breakthrough in early detection and treatment.
Researchers discovered a new way to trigger self-destruction of certain cancer cells by targeting specific molecules. By blocking the action of a protein called mTOR, scientists can activate apoptosis in cancer cells lacking a gene called p53, leading to cell death.
A new study by University of Michigan researchers reveals that protein RKIP governs prostate cancer cells' ability to enter nearby blood vessels, a crucial step in metastasis. Tumors with normal RKIP levels appear unable to invade blood vessels, while those without RKIP are more likely to spread.
Scientists discover that cellular senescence involves packaging of specific chromosomal regions into heterochromatin, which triggers a 'stop growing' response in cells. The study reveals genes are switched on in proliferating cells but silenced during senescence.
Researchers at UT Southwestern Medical Center have partially uncovered the stages in the elimination of viral infections and cancer cells by the human immune system. The study found that natural killer cells and cytotoxic T cells use different mechanisms to kill target cells, with significant differences in their roles and receptor usage.
Researchers discover cadmium inhibits DNA repair mechanisms, leading to dramatic mutations and increased cancer risk in humans. Environmental exposure to cadmium may cause genetic damage through this novel pathway.
Researchers have discovered that equine cloning can provide insights into human cancer causes, particularly in relation to calcium levels within cells. The study found that horses have lower intracellular calcium and slower cell activity rates compared to humans, which may contribute to their lower mortality rate from metastatic cancer.
A recent study found that whey protein increased glutathione levels in human prostate cells by up to 64%, potentially protecting against prostate cancer. Whey contains the amino acid cysteine, essential for producing glutathione, which helps control free radicals.
Blocking the activation of Stat5 in prostate cancer cells triggers extensive cell death, providing a new targeted therapeutic approach to manage cancer growth and metastasis. Prostate cancer is the second leading cause of cancer death in men, with approximately 220,900 new cases expected in the US in 2003.
Researchers have developed microgel polymer beads that can be engineered to break apart in acidic conditions, releasing vaccine antigens on the surface of immune cells. This technique avoids destroying protein antigens with stomach acids, making it a promising approach for future vaccines and gene therapy.
Researchers found that a bacterial enzyme, peroxiredoxin, controls the balance of hydrogen peroxide in cells. The enzyme regulates hydrogen peroxide levels to prevent damage while allowing it to signal important cellular processes.
Researchers found that ovarian cancer cells produce collagen VI, which remodels their environment to make them more resistant to chemotherapy. This could lead to new therapeutic interventions to overcome chemotherapy resistance and improve survival rates for women with ovarian cancer.
Researchers have developed a novel screening technique that quickly identifies chemical compounds active only against certain cancer-causing genes and proteins. This approach opens the door to custom-tailoring chemotherapy and may lead to more effective treatments for specific types of cancer.
Researchers at Virginia Tech have designed a new class of molecules that can bind to and stop replication of DNA when triggered by light. The complex molecules, developed by Professor Karen Brewer's group, have demonstrated the ability to kill cells in the presence of light.
A new study reveals that ATR kinase plays a crucial role in maintaining genome integrity by regulating cell cycle checkpoints and preventing DNA damage. The study shows that ATR is essential for ensuring cells leave the cell cycle without DNA damage, which can lead to diseases such as cancer.
Researchers at Georgetown University Medical Center found that malfunctioning beta-spectrin genes cause defects in embryonic development and interfere with TGF-beta functions, which are crucial for growth and cancer progression. This discovery has important implications for human disease research and treatment.
A recent study found that a rare genetic disease is caused by the shortening of telomeres, leading to premature aging symptoms like hair loss and slow wound healing. The researchers discovered that telomere dysfunction disrupts chromosome function, resulting in cellular chaos and organ failure.
Researchers found that cancer cells can migrate through protein matrices by reverting to a more rounded shape, allowing them to continue moving even when inhibitors are present. This 'salvage' pathway could be targeted by new drugs to combat cancer spread.
Researchers identified a protein called CUGBP2 that regulates the production of COX-2, a key culprit in arthritis and cancer. When CUGBP2 levels are high, it triggers cancer cell death by inhibiting COX-2 production.
A breakthrough discovery by Saint Louis University researchers reveals how the protein Bre1 functions in normal cells, shedding light on its role in cancer development. The study suggests that understanding this protein's regulation of gene expression could lead to new ways to block cancer-causing pathways.