Articles tagged with Cancer Cells
Whitehead Institute scientists report that the FLCN protein acts as a trigger to activate the mTORC1 pathway, which regulates cell growth in response to nutrient levels. This unexpected finding may provide insight into how cancer cells distort normal cellular functions to maintain their own harmful ways.
Researchers at the University of Nottingham have found a type of archaea that can reproduce without normal replication processes, growing faster in its absence. This discovery challenges existing understanding of DNA replication and has implications for cancer research.
Researchers at Boston University School of Medicine suggest epigenetics as a target for cancer therapy. Epigenetic changes mediate the development of cancer progenitor cells, which can grow rapidly to become full-fledged cancer.
The Cell-CT platform detected lung cancer in patient sputum samples with a sensitivity of over 95% and specificity of 99.8%. The technology creates comprehensive 3D digital images of cells, making it possible to determine the presence or absence of cancer with great accuracy.
Researchers discovered that individual molecular muscles within cells respond differently to various forces, shedding light on how cells 'feel' their environment. A computer model predicts cell behavior in response to altered levels of these molecules, with implications for understanding cellular disorders like cancer and neurodegenera...
Researchers at UCSF have discovered a new way to target cancer by controlling cell growth and boosting protein production during the S phase of the cell cycle. This study has implications for the development of new cancer therapies.
Researchers discovered distinct EBV subtypes with varying public health risks, including a strain associated with nasopharyngeal carcinoma. This finding highlights the importance of tailoring prevention efforts to specific viral strains.
Researchers at CNIO's Cell Division & Cancer Group have discovered that the protein Greatwall is essential for preventing mitotic collapse in mammals. By inhibiting Greatwall, cells can no longer divide properly, which may lead to slowed-down cancer growth and potentially reactivated tumour suppressor PP2A
A study finds that chronic myeloid leukemia cells with activating beta-catenin mutations are highly aggressive and resistant to Imatinib. Combined treatment with drugs restoring IRF8 expression and inactivating beta-catenin may prevent fatal leukemia progression.
A team of engineers has developed a new approach that marries computer vision and hardware optimization to sort cells up to 38 times faster than current techniques. The approach improves on imaging flow cytometry, which uses camera mounted on a microscope to capture cell features.
A study at the Weizmann Institute suggests that in a quarter of all leukemias, cancer cells use a balance between a mutated gene and its normal counterpart to keep going. The healthy RUNX1 gene plays a crucial role in blood cell development and maintenance.
A phase I clinical trial has shown that an anti-PD-L1 monoclonal antibody can produce striking responses in non-small cell lung cancer patients with metastatic disease who have failed to respond to previous chemotherapy. Smokers and former smokers are more likely to benefit from this treatment.
Researchers found that men with variable telomere length in cancer cells and shorter telomeres in stromal cells were more likely to develop metastatic disease and die sooner from their prostate cancer. This combination could be a marker for prostate cancer prognosis.
Cancer researchers at UC San Diego isolated and characterized early-stage prostate cancer cells, which may drive recurrent disease. The study suggests that these cells could be targeted for new treatments, potentially reducing cancer progression.
A team of U-M neuroscientists reports that SIRP alpha plays a critical role in stabilizing the most active synaptic connections between brain cells. This finding may aid research on conditions like autism, schizophrenia, and intellectual disability, which are linked to abnormal synapse function.
The circadian clock enables cells to use stored fuel efficiently when we fast, with NAD+ and Sirtuin 3 playing a critical role. Disrupting the clock leads to metabolic disorders, but providing NAD+ supplements can restore mitochondrial function.
A study published in the Journal of the National Cancer Institute found that proteins delivering leucine to prostate cancer cells are therapeutic targets. Inhibition of these proteins inhibits nutrient signaling pathways and over 100 metastasis-related genes, leading to cell cycle inhibition and reduced tumor growth.
Scientists at A*STAR's Singapore Immunology Network have discovered a new mechanism involving p53, the famous tumor suppressor, to fight against aggressive cancers. The strategy works by sabotaging cancer cells' ability to hide from the immune system, opening a new avenue for targeted therapy.
Scientists at the University of Copenhagen have identified a specific sugar molecule that aids in the growth of cancer cells. The discovery, published in PNAS, could lead to new ways to diagnose and treat cancer.
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.