Articles tagged with Cancer Cells
Cancer cells exploit a vicious cycle of mucus production to protect themselves from the immune system and promote tumor growth. Researchers at Rice University have identified a potential therapeutic target in rosiglitazone, a diabetes medication that can attenuate this cycle.
Researchers have discovered a network of genes in stem cells that foster cooperation, which is essential for the development and function of multicellular organisms. The study suggests that understanding this genetic mechanism could lead to new ways to address diseases such as cancer and immune system dysfunction.
Researchers at Dartmouth's Geisel School of Medicine discovered that cyclin A plays a crucial role in ensuring faithful chromosome segregation during cell division. In contrast to normal cells, cancer cells often fail to correct errors, leading to abnormal numbers of chromosomes and resistance to chemotherapy treatments.
Researchers developed a new system to test how viruses interact with cells in the body, revealing insights that will improve viral therapy. The technology allows for the use of real viruses in real environments, enabling scientists to study host targets for antiviral drugs.
Medical scientists at the University of Alberta have made a key discovery about how the immune system kills healthy cells while attacking infections. Their research could lead to better solutions for cancer and anti-viral treatments by manipulating the immune system response to block collateral damage.
Scientists discovered a new weakness in cancer cells that makes them more susceptible to chemotherapy by targeting the HDAC5 protein. Cancer cells with longer telomeres tend to be resistant to therapies, while shorter telomeres make them more vulnerable to treatment.
St. Jude Children's Research Hospital scientists have identified a protein that blocks death of high-risk acute lymphoblastic leukemia cells, leading to a new two-drug combination therapy approach. The study shows promise for treating Ph-positive ALL, a high-risk cancer with limited treatment options.
Researchers uncover how ABL regulatory unit controls cell fate in CML, with implications for cancer treatment. The study finds that anchoring ABL on the cell membrane is essential for apoptosis, highlighting a potential target for novel therapies.
Research reveals that chromosomal rearrangements, such as inversions or translocations, can be beneficial in certain environments, leading to improved growth abilities. This discovery sheds light on how natural selection shapes chromosome structure to favor specific conditions.
Researchers found that a combination of calorie restriction and targeted therapy may increase cancer survival. Calorie restriction decreased Mcl-1 protein activity, sensitizing lymphoma cells to treatment. This study suggests a potential new approach to improve cancer treatment efficacy.
Researchers found that flavonoids in celery, artichokes and Mexican oregano can kill human pancreatic cancer cells by inhibiting the GSK-3β enzyme. This pre-treatment approach may prolong life without curing the disease, while preventing it could reduce cancer risk with chronic flavonoid exposure.
Researchers at CWRU School of Dental Medicine have discovered the link between an oral bacterium and colorectal cancer. They found that Fusobacterium nucleatum can trigger cancerous cell growth by modulating E-cadherin/ß-catenin signaling.
Researchers have produced detailed descriptions of human folate receptor proteins, aiding in the design of new drugs that can target cancer cells without harming healthy ones. The findings could lead to effective treatments for ovarian cancers and inflammatory diseases such as rheumatoid arthritis.
Researchers have discovered a key role played by TACC3-ch-TOG-clathrin in forming inter-microtubule bridges that stabilise kinetochore fibres during mitosis. Removing this protein team can induce cells to arrest and die, potentially providing a new approach to cancer treatment.
Researchers at Columbia University Medical Center created DNA nanorobots that can identify and tag specific human cells based on multiple surface proteins. This allows for precise targeting of cancer cells with minimal impact on healthy cells, potentially revolutionizing cancer treatment.
Researchers at Mayo Clinic have made a breakthrough discovery about the origin of inflammation-driven pancreatic cancer. They found that chronic inflammation in the pancreas can push acinar cells to transform into duct-like cells, which can then acquire mutations leading to further progression of pancreatic cancer. The study identified...
Researchers found cancer cells can reverse replication forks using 'fork reversal' repair after DNA damage caused by topoisomerase I inhibitors. This process is controlled by proteins PARP and RECQ1, which could be targeted for effective treatment with lower toxic side effects.
UPCI researchers discovered that targeting 'cell sleep' can kill a larger fraction of cancer cells, increasing the effectiveness of cancer drugs. This finding has implications for gastrointestinal stromal tumors (GISTs), which are often treated with targeted therapy drug imatinib.
Scientists at Cancer Research UK have discovered a new molecule that prevents cancer cells from responding to low oxygen levels, targeting the master switch HIF-1. The researchers developed this approach using synthetic biology and testing over 3.2 million potential compounds.
Researchers have identified a new therapeutic target by linking protein translation to heat shock response in cancer cells, which slows tumor growth and makes drug-resistant tumors vulnerable to other therapies. A compound called Rohinitib disrupts this link, normalizing metabolism and killing cancer cells.
Researchers found that ovarian cancer cells colonize milky spots in the omentum, which promotes cell growth and spread. The study suggests an alternative model of omental colonization, where both milky spots and fat cells play a role in attracting cancer cells.
A LSUHSC researcher has been awarded a five-year, $1.5 million NCI grant to investigate the connection between chronic inflammation and cancer development. The project aims to understand how p53 dysfunction in normal cells surrounding cancer cells can lead to an inflammatory microenvironment that supports tumor growth.
A team of international researchers has identified a self-perpetuating signaling circuit in connective tissue cells that allows them to form a front and back and propel themselves in a particular direction. This propulsion is similar to the movement used by tumor cells to invade healthy tissue during cancer metastasis.
A study by Weill Cornell Medicine found that even healthy-looking smokers have damaged airway cells with characteristics similar to those in aggressive lung cancer. The researchers discovered that these cells express human embryonic stem cell genes, which are normally only active in developing embryos.
Researchers have discovered a way to kill cancer cells by blocking a specific protein that enables them to survive nutrient starvation. This breakthrough could lead to a more targeted and effective treatment for various types of cancer.
Researchers have gained groundbreaking knowledge about proteases, enzymes that play a role in cancer cell development. The study reveals that proteases can bind to each other instead of just cleaving, which may lead to the development of new anticancer drugs.
A team of scientists at the Salk Institute for Biological Studies has identified a critical pathway in cell cycle control that, when disrupted, leads to cancer cell proliferation. Shortened telomeres, which occur with cellular aging, activate a DNA damage response that arrests cell growth.
Researchers have developed a new method for identifying cell of origin of proteins in multicellular environments, enabling comprehensive mapping of cell-cell communication. This technique, CTAP, exploits amino acid biosynthesis and stable isotope labeling to link proteins directly to specific cell types.
Researchers at UTMB found that colon cancer cells produce large amounts of hydrogen sulfide, which they use to make energy and grow. Blocking the production of this compound, CBS, was shown to curb tumor growth in mice.
Scientists have successfully targeted a malfunctioning immune system enzyme to eliminate diseased cells from patients with myelodysplastic syndrome (MDS), a blood disorder and precursor to leukemia. The research provides a molecular target for designing new drugs, offering a promising treatment option.
Researchers identify unique properties of K11-linked polyubiquitin chains, suggesting new cellular processes involved in disease maintenance. These findings may lead to novel treatments for diseases like cancer and diabetes.
Cancer originates from a default genetic 'safe mode', where cells revert to an ancient programming, leading to uncontrolled proliferation. The theory suggests that cancer-causing genes are reactivated in adulthood due to triggers like chemicals or radiation, adding weight to the radical new idea.
Researchers at the Buck Institute manipulated a signaling pathway implicated in Barrett's esophagus, suggesting a change in stem cell function as the cause of this transformation. This discovery may lead to new targets for therapies and inform the development of more effective treatments for Barrett's esophagus.
Researchers discovered that forced telomere elongation promotes cancer cell differentiation, suppressing genes involved in tumor malignancy. Telomeres may modulate cell behavior by controlling gene expression, potentially leading to new cancer treatments.
A recent study published by researchers at Penn State College of Medicine found that protein km23-1 is crucial for the spread of colon cancer cells. The team discovered that reducing km23-1 levels decreases the production of TGF-beta and reduces a framework structure associated with cancer cell movement.
Researchers at MIT have discovered a mechanism that allows cells to read their own DNA in the correct direction and prevents most of the so-called 'junk DNA' from copying into RNA. This process helps explain the existence of many recently discovered types of short strands of RNA whose function is unknown.
Researchers at Harvard School of Public Health discovered that cells move in a group, propelled by forces from within and nearby cells, to fill spaces. This phenomenon, dubbed 'kenotaxis,' could improve understanding of disease mechanisms and inform potential drug targets.
Researchers at Scripps Research Institute receive $1.4 million from the National Cancer Institute to create a potential new drug targeting malignant cells in CLL, while sparing normal tissues. The study aims to deliver cytotoxic drugs with specific targeting using cell surface receptor TOSO and receptor tyrosine kinase ROR1.
Researchers at UT Dallas discovered that lung cancer cells consume more oxygen and synthesize a critical chemical called heme, which can be exploited to inhibit cancer growth. Inhibiting heme synthesis affects lung cancer cells' ability to proliferate and migrate.
A study by UCSD researchers reveals that MCL-1 promotes normal heart function, but its absence leads to rapid heart failure and cell death. The protein's role in cancer treatment and potential cardiac toxicity are also explored.
Researchers describe 'chase and run' cell movement mechanism that explains process of metastasis. Cancer cells recruit healthy cells using small chemical molecules, promoting directional collective migration.
Researchers used advanced mathematical modelling to devise strategies for making cancer cells exquisitely sensitive to virus infection, killing them without affecting normal cells. The models were remarkably accurate, predicting experimental outcomes in a mouse model of the disease and creating a useful framework for further research.
Researchers at Uni Basel have discovered Sox4 as a key player in cancer metastasis, triggering the epithelial-mesenchymal transition (EMT) process. The study found that Sox4 promotes the expression of genes involved in EMT and metastasis, leading to changes in gene expression and cell behavior.
Researchers at the University of Copenhagen have discovered a new way cells communicate with each other using antennae-like structures called primary cilia. This breakthrough sheds light on the causes of debilitating diseases such as heart defects and birth defects, highlighting the importance of TGFβ signalling in fetal development.
Researchers at UCLA have isolated a new population of pluripotent stem cells, called Multi-lineage Stress-Enduring (Muse-AT) cells, from fat tissue that can differentiate into virtually every cell type in the human body. These cells are stress-resistant and may even be activated by severe stress, making them potentially superior source...
Researchers at the University of California, San Diego School of Medicine discovered a novel mechanism that suppresses tumor growth by stabilizing heterochromatin, a form of chromosomal DNA. This finding suggests a potential new approach to inhibit cancer gene expression and may represent a new class of tumor suppressors.
Researchers have captured the first three-dimensional crystalline snapshot of the initial step in actin filament formation, crucial for understanding cell shape and cancer. The study's dual-mutant approach helped overcome challenges in forming crystals, revealing critical contacts involved in nucleation.
Researchers at Monash University have identified a sub-group of cells that can contribute to prostate cancer recurrence, opening up new treatment options. These previously unidentified cells are potential targets for future therapies and may be targeted before the cancer reaches an incurable stage.
Researchers developed a novel approach to make ovarian cancer cells susceptible to an antitumor drug, potentially improving treatment outcomes. The strategy targets telomeres and shows promise in treating other epithelial cancers.
Researchers have identified two ruthenium-based complexes that target cancer cells more effectively and are less toxic than current chemotherapies. The complexes, which seem to target cells in hypoxic states, could complement widely used platinum-based therapies like cisplatin.
Researchers at the University of Montreal have discovered how rapamycin prevents cells from dividing, potentially slowing cancer progression and other diseases of abnormal growth. The study reveals that TOR sends a signal to shut down B cyclin production through an intermediary protein.
Researchers at LMU discover how cellular respiration generates reactive oxygen species that can cause DNA mutations, leading to cell dysfunction and cancer. The study highlights the importance of improving treatment options for cancer by inhibiting DNA repair processes in tumor cells.
Researchers successfully targeted doxorubicin to mitochondria, killing cancer cells even those with developed pumps. The study suggests this approach could work with other nucleus-targeting anti-cancer drugs.
Mayo Clinic researchers found that positively charged gold nanoparticles can be effective against ovarian cancer cells when their cellular stress is increased. This is achieved by inhibiting calcium uptake into the mitochondria, which helps to make the nanoparticles more effective in destroying cancer cells.
Scientists discovered that a molecule called BRD4 recognizes a specific amino acid on NF-kappa B and activates it, preventing its degradation in cancer cells. This interaction is critical in the development of cancer, and blocking it may lead to new cancer treatments.
A new computational method called viSNE enables scientists to analyze high-dimensional cancer data, revealing distinct cell subpopulations and detecting minimal residual disease. This breakthrough technology has the potential to improve cancer diagnosis and treatment.
Researchers at Memorial Sloan-Kettering Cancer Center have discovered that expression of TRAIL in transplanted hematopoietic stem cells is critical for an effective anti-tumor response. This finding has led to the development of new therapeutic strategies to suppress graft-versus-host disease while maintaining anti-tumor activity.
Researchers at MIT have identified ALKBH7 as a key protein involved in programmed necrosis, a cell death pathway that can help prevent cancer cells from surviving DNA damage. By mimicking the effects of this protein, drugs may be able to induce necrosis in resistant cancer cells, providing a new potential target for cancer treatment.
A team of researchers at NYU School of Medicine has made a breakthrough in understanding how pancreatic tumor cells feed themselves. By identifying the role of macropinocytosis in delivering nutrients to Ras-transformed cancer cells, they have uncovered a potential new target for treating this lethal disease.
A new study reveals distinct characteristics between inducible and natural IL17-producing T cells, with different signals required for cytokine production. The findings suggest a specific role of Akt protein complex in regulating cytokine production by these cell types.