Articles tagged with Cancer Cells
A Phase III clinical trial of Tarceva and chemotherapy showed no overall benefit in survival or response, but a subgroup analysis found young non-smokers treated with Tarceva survived longer than those using chemotherapy. The study suggests that this class of drug may not function well when combined with chemotherapy.
A novel therapeutic bortezomib combination will be tested in a phase II trial for advanced non-small cell lung cancer. The regimen, combining bortezomib with gemcitabine and carboplatin, shows promise in preclinical research, where giving bortezomib last may enhance its effectiveness.
Researchers at UC Davis Cancer Center discovered that sequential administration of erlotinib and docetaxel enhances effectiveness in treating non-small cell lung cancer. The study showed that giving docetaxel first, then erlotinib, was more effective than simultaneous or alternative administration.
Researchers have found a novel agent, SU11248, to be highly effective in treating advanced renal cell carcinoma. The treatment has shown significant activity in patients whose cancer had failed to respond to standard therapy.
A study by Rockefeller University researchers reveals that a single molecular pathway controls both cell growth and death in a type of lymphoma cancer. The NF-kappa B signaling pathway, responsible for promoting cell growth, also regulates the p53 tumor suppressor protein's function, which normally destroys harmful cells.
Researchers identified more than 500 proteins contained in the midbody structure necessary for normal cell division. Inactivating these proteins led to cytokinesis defects, causing abnormal cell division, which can lead to diseases such as cancer, birth defects, and neurological disorders.
A study published in EMBO Journal found that resveratrol, a compound in grape skins, can starve cancer cells by inhibiting the action of NF-kB. This inhibition leads to apoptosis, or cell death, in cancer cells. Resveratrol's effectiveness against cancer is linked to its ability to block NF-kB's inflammatory response.
Scientists at Brown University have identified two molecular mechanisms that trigger senescence in aging cells. The discovery of p16, a protein that operates independently from telomeres, provides new insights into the regulation of cell division and holds promise for the development of therapeutics to manipulate these targets.
Researchers at Duke University Medical Center have identified a protein called Hypoxia Inducible Factor (HIF-1) as the master switch that enables blood vessels to survive and nourish remaining cancer cells after radiation therapy. By suppressing HIF-1 with experimental drugs, they successfully inhibited tumor growth in animals.
Researchers at SLU have developed oncolytic adenoviruses that target specific types of cancer cells, such as colon and lung cancer. These engineered viruses attack and destroy cancerous cells through a mechanism different from chemotherapy or radiation.
Researchers find that alkylating agents can induce necrotic cell death in cancer cells by damaging DNA and activating the PARP protein. This process is specific to proliferating cancer cells and does not affect healthy cells, offering a potential new approach to treating cancer.
Vanderbilt University Medical Center students James Peacock and Olga Weinberg have been awarded HHMI fellowships to pursue research in immunology and estrogen receptors. The fellowships will enable them to conduct academic-year-long research projects culminating in the Meeting of Medical Student Fellows.
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.
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.
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.
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.