Articles tagged with Cancer Cells
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.
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.
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.
New tri-metallic supra-molecules can be positioned in exact parts of cancer cells and excited by therapeutic light to kill diseased cells. The system enables precise targeting, reducing side effects of chemotherapy.
Cells utilize an enzyme called the proteasome to remove unnecessary proteins. The study found that the proteasome can independently degrade substrates involved in Parkinson's disease and some types of cancer, producing fragments reminiscent of pathological deposits in Parkinson's patients.
Scientists discovered that SNF5 is a tumor suppressor gene responsible for malignant rhabdoid tumors, a rare and aggressive childhood cancer. The study used a novel knockout technique to create mice with reversible, inverting conditional SNF5 genes, which developed cancers quickly.
Researchers found that overexpressed LPAAT-beta is highly tumorigenic and causes cancer cells to die when inhibited. The small molecule inhibitors induce apoptosis in various tumor cell lines, including lung and colon cancers.
Scientists at Stanford University have created synthetic DNA nanocircles that can lengthen telomeres in test tube cells, a key factor in determining cell lifespan. This breakthrough could lead to the development of new methods for studying aging and cancer, as well as alternative approaches to transplantation medicine.
Researchers from the University of Pittsburgh found that KSHV, a known carcinogenic virus, inhibits immune function and causes cancerous cells to grow through a hormone-like substance called vIL-6. This discovery reveals an overlap between the immune system and tumor suppressor pathways targeted by KSHV.
Researchers at Johns Hopkins University have identified a complex signaling pathway that regulates gene activity in living cells. The discovery reveals that the timing of signal transmission plays a critical role in determining which genes are activated, and could lead to the development of new medications targeting cancer cells.
Researchers at UW-Madison have identified the PIPKI?661 enzyme as a promising target for preventing cancer cells from metastasizing. By inhibiting this enzyme, cancer cells' ability to migrate to other parts of the body can be blocked.
Researchers designed a DNA vaccine that stimulates the immune system to recognize and attack proliferating blood vessels in tumors, depriving them of oxygen and nutrients. The vaccine has shown promise in preventing effective angiogenesis and inhibiting tumor growth, offering potential for novel cancer therapies.
A new strategy in cancer treatment involves using genetic information to guide drug delivery, allowing for more targeted and efficient treatments. The approach uses nucleic acid-triggered catalytic drug release, recognizing and responding to unique cancerous sequences to deliver potent anticancer drugs.
Gene Network Sciences will use the federal grant to learn how pharmaceuticals work against cancer cells, creating computer models to identify nontoxic drug targets. The company aims to make drug-discovery more predictable for pharmaceutical and biotech companies with its new technology.
A study published in Immunity reveals that the MEF protein plays a critical role in the development and function of natural killer cells, which can recognize and kill cancer cells. The findings provide a new target for therapeutic interventions, potentially improving bone marrow transplant strategies.
Researchers at the Norwegian Cancer Society have discovered that certain types of fish fat contain compounds with anti-cancer properties. The study suggests that these compounds may be used to develop new treatments for various types of cancer.
Researchers at Memorial Sloan Kettering Cancer Center discovered that cancer cells containing high levels of Myc protein cannot activate p21 gene production, leading to cell death. The study's findings suggest a potential strategy to increase chemotherapy effectiveness by favoring apoptosis over citostasis.
Research highlights increased cervical cancer risk in smokers, while ovarian tumors with BRCA2 mutations also commonly have BRCA1 mutations. A potential therapeutic approach for eliminating malignant urothelial cells is also explored through CD40 ligation.
Researchers at UNC Chapel Hill used nuclear magnetic resonance spectroscopy to study the effects of crowded environments on protein shape. They found that intrinsically unstructured proteins exhibit a definite folded-up shape when inside cells, unlike their apparent lack of structure in water solutions.
Researchers have isolated a key component of cell death signals that can be targeted to prevent cancer growth. By understanding how these signals interact, scientists hope to develop new anti-cancer therapies.
Cancer cells have evolved to continually activate telomerase, keeping telomeres intact and enabling rapid division. Researchers at UC Berkeley are now searching for proteins and signals involved in telomerase shuttling around the cell nucleus to develop new therapeutic strategies.
Researchers at University of Illinois Chicago have discovered a way to render cancer cells more susceptible to immunological attacks and chemotherapy. By inserting the E1A gene into malignant cells, they can prevent tumor cells from blocking immune defenses, paving the way for new treatments.
Researchers at Hebrew University have developed a novel technique that uses an engineered virus to induce cancer cells to activate PKR protein, causing them to self-destruct. This innovative approach has shown promising results in halting the spread of brain tumors and offers a new direction for cancer treatment.