Articles tagged with Cancer Cells
A team from the University of Pennsylvania School of Medicine has identified a molecular master switch for pancreatic cancer, which could serve as a potential predictor of treatment outcome. The researchers found that Prrx1 and Sox9 regulate the emergence of an intermediate cell type that can give rise to cancer.
Early-onset prostate cancer is linked to high levels of androgen receptor activity in young patients, leading to gene rearrangements that promote cancer. This discovery could lead to new diagnostic, prognostic, therapeutic, and prevention strategies for the disease.
Scientists at Virginia Commonwealth University Massey Cancer Center discovered a novel combination of drugs that selectively destroys lymphoma cells through apoptosis. The experimental therapy combines ibrutinib and bortezomib, with the latter being relatively non-toxic to healthy cells.
A previously poorly investigated signalling pathway is crucial for prostate cancer cell proliferation, involving the production of cAMP at multiple locations in the cell. Inhibiting the soluble adenylyl cyclase enzyme suppresses cancer cell growth, suggesting a promising new therapeutic approach.
Researchers at Stanford University School of Medicine have discovered an antibody that can inhibit the growth of gastrointestinal stromal tumor (GIST) cells resistant to other treatments. The antibody targets KIT receptor mutations, stimulating immune cells to kill rogue cells.
Scientists have visualized molecular changes in a critical protein involved in cell death, providing new insights into apoptosis and its role in disease. The discovery could lead to the development of new medicines that control cell life or death.
A research team in Japan has developed a new imaging method that allows for detailed intracellular temperature maps, revealing the temperature difference varies greatly depending on the location in the cell. This breakthrough may lead to a better understanding of diseases like cancer and its pathogenesis.
Researchers use picosecond ultrasonics to probe human cells' stiffness and viscosity, predicting potential applications in medical implants and cancer research. The technique could help identify cell disease and monitor cell activity without damaging the cells.
Researchers at Sanford-Burnham Medical Research Institute discovered that tumors lacking the protein PKCζ can survive on alternative nutrients. The study suggests glucose depletion therapies may work against these tumors as long as they produce PKCζ, which is responsible for tumor metabolism.
Researchers at Georgia State University have identified a new target to stop cancer's spread, targeting the interaction between two proteins in cells. Disrupting this interaction inhibits metastasis and has implications for treating various diseases.
Silibinin kills UVA-damaged cells, protecting against DNA damage. It also protects human skin cells from UVB radiation by increasing expression of interleukin-12, promoting cell repair.
Researchers discover gene FBH1 crucial for chemotherapy's effectiveness in killing cancer cells. By understanding the role of FBH1, doctors can tailor treatment to individual patients based on genetic fingerprint.
Scientists have discovered that superoxide dismutase (SOD1) regulates cell energy and metabolism, preventing uncontrolled cell growth associated with cancer. This enzyme also protects cells from free radical damage.
A new technique called Bru-Seq allows researchers to label newly created RNA, enabling them to analyze the synthesis and stability of RNA in cancer cells. This breakthrough has the potential to provide deeper insights into gene expression and identify early warning signs of disease.
Researchers at the National Cancer Centre Singapore have discovered a crucial link between mutant p53 genes and reduced treatment response in cancer patients. The dominant-negative effect of these mutations inhibits tumor suppressor activity, leading to poor responses or earlier relapse after treatment.
A team of scientists has discovered quadruple helix DNA structures in human cells, which may be a new target for cancer treatment. The discovery was made using fluorescent biomarkers and shows clear links between quadruplexes and DNA replication.
The study found that CD4 helper T cells can transform into killer cells by overcoming a suppression mechanism triggered by a transcription factor. This transformation enables the helper cells to take on the role of killer cells in mounting an immune attack against viruses, cancerous tumors, and other damaged or infected cells.
Autophagy is triggered when cells are starved for nutrients, infected, or damaged. The study reveals that AMPK regulates Vps34 kinase complexes in different ways, inhibiting non-autophagy enzymes and activating autophagic ones.
Researchers discovered that grape seed extract selectively targets advanced colorectal cancer cells with fewer genetic mutations, leading to increased effectiveness in treatment. The compound induces oxidative stress and programmed cell death, reversing its effects when antioxidants are present.
Researchers aim to develop better ways to treat patients by eliminating all cancer cells and avoiding disease relapse. They will study how cancer cells evade treatment by hiding in protective compartments inside the body.
Researchers found that blocking a particular pathway in cancer cells makes it easier for common drugs to annihilate tumors. By targeting this pathway, scientists aim to enhance the impact of current therapies and design new drugs to disrupt it.
Researchers at McGill University have discovered AMPK's role in restricting cancer cell growth by regulating metabolism and preventing the use of sugar to fuel growth. AMPK, a tumour suppressor, can help control tumour development by targeting energy levels and promoting healthy cellular function.
Researchers at Johns Hopkins Medicine have developed a novel approach to sorting out cancer-causing genetic mutations in cancer cells. By testing proteins produced by genes with random mutations, they created a catalog of mutants with cancer-promoting potential. This could lead to more personalized treatment strategies for patients.
Researchers have identified 7 new genes with a key role in T-ALL, a form of leukemia primarily affecting children. The study also found that defects in the ribosome can play a role in cancer activation, offering potential new targets for treatment.
Researchers found that cancer cells use unfolded protein response (UPR) to manipulate immune cells, making them ineffective against tumors. Tumor cells exploit UPR to promote their survival and growth, and this mechanism is being targeted for potential therapy and improved cancer vaccines.
Researchers at Penn State College of Medicine found that targeting km23-1, a motor protein involved in cell migration, can slow the spread of cancer cells. By inhibiting km23-1, cancer therapies may be developed to prevent tumor cells from migrating to other parts of the body.
The American Society for Cell Biology's Celldance awards recognized top videos showcasing cellular mechanisms in development, health, and disease. Winners included a time-lapse of fruitfly embryonic development and a cancer cell movement video.
Researchers discover that cells under oxidative stress deposit oxidized glutathione in a cellular waste repository called the vacuole, protecting themselves from damage. This finding challenges previous assumptions about oxidative stress and its link to various diseases.
Researchers have discovered a new type of cell division called klerokinesis, which appears to be an evolutionary failsafe mechanism that could rescue cell functions during embryonic development. By analyzing human retinal pigment epithelial cells, the team found that klerokinesis can help maintain genomic integrity and potentially prev...
Cedars-Sinai researchers have successfully converted ordinary heart cells into pacemaker cells using a single gene, Tbx18. The new cells generate electrical impulses and are indistinguishable from native pacemaker cells, offering a potential alternative to electronic pacing devices.
Researchers have developed a new technique to create targeted immunotherapies for cancer, recognizing antigens on cancer cells that are not found on healthy cells. The approach uses chimeric antigen receptors (CARs) and costimulatory receptors (CCRs), allowing T cells to attack specific types of cancer cells while sparing normal cells.
Researchers at the University of Alberta have identified a rare type of cancer suppressor that can trigger cell death when targeted. By inactivating this gene, cancer cells are destroyed while healthy cells remain intact.
Researchers at Baylor College of Medicine have discovered a vegetable compound that can reduce the number of acute lymphoblastic leukemia cells. Sulforaphane, found in broccoli and other cruciferous vegetables, was shown to kill cancer cells while leaving healthy cells unaffected in lab tests.
A team of investigators has identified a previously unknown mechanism regulating oncogene-induced senescence (OIS), a natural response to tumor development. Down-regulation of deoxyribonucleoside pools causes DNA damage, leading to cell cycle arrest and senescence. Restoration of depleted dNTP pools can suppress DNA damage and OIS.
In pre-clinical experiments, Angiocidin reduced acute myeloid leukemia (AML) cells by almost two-thirds, demonstrating its potential as a safer treatment alternative to standard-of-care chemotherapy agents like Ara-C. The protein also stimulated maturation in affected white cells, causing them to behave like normal cells.
A University of Colorado Cancer Center review suggests rice bran offers anti-cancer properties due to its synergistic bioactive compounds. The clinical trial tests rice bran's effectiveness in preventing colon cancer recurrence, with researchers exploring the optimal composition and daily intake for chemoprevention.
Scientists at Johns Hopkins Medicine used a synthetic molecule to stimulate cell movement, bypassing the cells' usual sensing mechanism. This breakthrough provides powerful tools for studying cell movement and its role in cancer progression and immunity.
The study, led by Peter Jones, identified specific genes that must be turned off for cancer cells to survive. The findings provide a new target for cancer treatments and may lead to more effective medicine.
Researchers at Rice University have developed a way to selectively kill some diseased cells while treating others in the same sample using tunable plasmonic nanobubbles. The process activates with a pulse of laser light and leaves neighboring healthy cells untouched.
Researchers identified a transporter molecule on the surface of cancer cells that can take in a toxic substance, allowing it to kill cancer cells. This discovery could lead to more targeted and effective cancer treatments.
Researchers at Scripps Research Institute determine the structure of two proteins that form specialized subunits within cells, crucial for maintaining cell health. This discovery has implications for developing new cancer therapies by inhibiting autophagosome formation.
A study by the University of Geneva reveals that colon polyps exhibit a 'mutator' profile associated with increased SNS mutations, leading to accelerated progression to malignancy. Three genes (APC, CTNNB1, and BRAF) are identified as initial causes on the road to cancer.
Scientists at IRB Barcelona created a Drosophila melanogaster fly model that reproduces the steps of healthy cell transformation into cancer. The model can help identify genes and molecules involved in cancer progression, potentially leading to specific treatments for cells with genomic instability.
Researchers discovered that acinar cells convert into duct-like cells that initiate tumors in pancreatic cancer. Inflammation of the pancreas promotes this conversion. The study suggests Sox9 as a potential target to prevent early tumor-initiating events.
Researchers at Scripps Research Institute discover a novel cell signaling process that improves immune cell function, potentially leading to new treatments for cancer and infectious diseases. The study identifies a key regulator of immune function and suggests the development of drugs that enhance Natural Killer cell activity.
A study published in Cancer Discovery reveals that microRNAs can modify gene expression, converting normal fibroblasts into cancer-associated fibroblasts that promote tumor growth. The researchers identified three microRNAs involved in this process and found that inhibiting these signals could disrupt the cancer's support system.
A UAlberta researcher has developed 'homing beacon drugs' that selectively kill cancer cells while sparing healthy ones. These smart drugs use nano-technology to identify cancer cells based on a unique protein found only in them, allowing for targeted treatment and potential reduction in side effects.
Researchers identified PUMA, NOXA, and TRB3 as executors of glutamine-starved cells in Myc-mutant cells. The team showed that drugs targeting these proteins induced cell death in assays using neuroblastoma cells and inhibited tumor growth in transgenic mice.
Researchers found that a protein called TGFβig-h3 is impaired in patients with gastric cancer, allowing cancer to spread. This discovery could lead to the development of new therapies restoring the functions of this protein.
Iowa State researchers identify three types of cell-to-cell bonds, each reacting differently to a pulling force. The findings, published in the Proceedings of the National Academy of Sciences, have implications for understanding diseases such as cancer and cardiovascular problems.
Researchers at Rensselaer Polytechnic Institute have developed an ultrasensitive method for detecting sugar molecules, known as Glyco-qPCR. This technique enables a more detailed understanding of cellular functions than genetic or proteomic information can provide, and has the potential to revolutionize the study of glycans.
Researchers at Scripps Research Institute have discovered new selective inhibitors of diacylglycerol lipases (DAGL), enzymes involved in making 2-AG, a key cannabinoid. Early tests suggest these compounds may also reduce pro-inflammatory molecules linked to rheumatoid arthritis, potentially leading to new therapeutic approaches.
Researchers found that nisin slows or stops tumor growth by interrupting the cell cycle in cancer cells but not healthy ones. The study's findings suggest that nisin triggers cell death through the activation of protein CHAC1, which is a new role for this protein.
Researchers discovered epigenetic marks drive development of three deadly white blood cell cancers, including BCR-ABL1-positive B-ALL. The study identified key biomarkers and potential treatments, such as targeting the CD25 protein and blocking cancer-driving genes like BCL6.
PARG, a molecule involved in DNA repair, has been found to regulate gene expression and modulate cell transcriptional activity. This discovery highlights the potential of targeting PARG in cancer treatment.
T-cells use protein signals to communicate with each other, with specific patterns and squishiness preferred. The discovery may help improve T-cell activation for immunotherapy and cancer treatment.
Whitehead scientists found that traditional approaches ignore differences in mRNA amounts between cells, which can lead to misinterpretations in cancer research. The team proposes using RNA spike-ins as a standardized control to eliminate assumptions.
Researchers at Salk Institute discovered adenovirus proteins that hijack cell machinery, including growth and replication. E4-ORF3 protein assembles into polymers that capture tumor suppressors and silence genes, providing a new avenue for cancer therapies.
Researchers developed a novel method to determine how ready acute myeloid leukemia (AML) cells are to die, helping cancer specialists choose treatments more effectively. The tool measures the 'primed to die' status of AML cells by apoptosis, allowing for better prediction of patient outcomes and personalized treatment decisions.
Researchers at Tel Aviv University develop RNA interference therapies to target the faulty gene CCND1, leading to the aggressive over-production of Cyclin D1. The treatment has shown success in human cells and is being tested in a mouse model with MCL.