Research on the cell biology of tumors. Covers cancer-cell vulnerabilities, tumor spread, nanoreactor therapies, and AI-guided cancer research.
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.
New research reveals that highly metastatic ovarian cancer cells are softer than less aggressive ones, suggesting cell stiffness as a valuable biomarker. This discovery could aid in the development of optimal chemotherapies for various types of cancer.
Scientists at USC have discovered a new type of drug that works by targeting Protein Disulfide Isomerase (PDI) in ovarian cancer cells. The drug, PACMA31, has shown promise in reducing the number of doses needed and making it effective for patients with resistant cancer.
A new study found that lactoferricin4-14, a milk protein, reduces colon cancer cell growth and DNA damage by prolonging the cell cycle and increasing DNA repair. This suggests that milk's cancer-preventive effects may be linked to its ability to promote DNA repair in normal cells.
Scientists focus on RNA processing differences in cancer cells to understand their role in tumor development. Alternative RNA splicing occurs more frequently in cancerous cells, but its biological importance is unknown.
Researchers found that DNp63a employs epigenetics to silence anti-proliferative genes, keeping cancer cells alive independently of p53. This discovery opens up new possibilities for targeting the protein's partner enzymes to break its cancer-causing mechanism.
Researchers developed a new method to identify proteins secreted by cells, eliminating drawbacks of traditional approaches. This technique isolates the 'secretory pathway' organelles and analyzes their contents using mass spectrometry, providing precise data on cell biology.
A new approach devised by EMBL scientists enables the distinction of proteins secreted by cells from those in their food, allowing measurement of secretion changes over time. This method has opened new avenues for drug and biomarker screening, as well as studying cell responses to drugs and 3D growth conditions.
Researchers have successfully imaged cells growing on spherical surfaces using a novel class of substrates. This technique has potential applications in cancer detection and treatment, as well as stem cell differentiation and tissue engineering.
Researchers at Northwestern University have identified two promising therapies to treat AMKL: alisertib and dimethylfasudil. Alisertib targets Aurora A kinase and shows promise in mouse models, while dimethylfasudil boosts mature bone marrow cells and inhibits malignant ones.
Researchers tested APR-246 on 22 patients with advanced blood or prostate cancer, finding indications that the substance restored p53 gene function and triggered cancer cell apoptosis. In two patients, tumor regression was observed, suggesting potential clinical benefits.
Scientists from CNIO describe natural selection at the cellular level, where tissues and organs select the 'best' cells to fend off disease processes. The study reveals the role of haemocytes in eliminating cell residues, shedding light on mechanisms of homeostasis and potential cancer detection.
Two new studies have identified novel genes and patterns of mutations involved in lung cancer, with significant differences found between smokers and non-smokers. These findings could lead to targeted therapies to improve survival rates and outcomes for lung cancer patients.
Researchers found a cellular cause of birth defects like cleft palates and missing teeth by blocking an ion channel that disrupts protein signaling pathways. This discovery may lead to the prevention of birth defects and has potential implications for cancer treatment.
Researchers at the University of Illinois have successfully infected various types of canine cancer cells with a pox virus while sparing healthy cells. The study's findings suggest that viral therapies could complement or replace standard cancer treatments, making it a promising approach for treating dog cancer.
Researchers at Dana-Farber Cancer Institute have found a small molecule, P5091, that triggers programmed cell death in drug-resistant myeloma cells. Combining P5091 with other therapies enhances its anti-myeloma effects.
Researchers found that standard chemotherapy with paclitaxel, carboplatin, and bevacizumab is equally effective as an experimental regimen in treating advanced non-squamous non-small cell lung cancer. The study suggests that both regimens are tolerable but have different toxicities.
A genome-wide scan of small cell lung cancers reveals an association between SOX2 gene amplification and aggressive disease. Overproduction of SOX2 proteins may ignite or sustain abnormal cell growth in the lung.
Researchers suggest a 'cyber war' on cancer by breaking the code of cancer cells' social behavior, similar to bacterial colonies. This approach could help prevent dormancy and reawaken cells for targeted chemotherapy attacks.
Researchers created a synthetic protein that binds to degraded collagen, which is often damaged by disease. This protein can detect cancerous cells, arthritis, and other diseases in the body. The technique may lead to new diagnostic imaging technology and treatment options.
Researchers have identified molecular compounds that activate a key enzyme, PKM2, which governs how cancer cells use glucose and its metabolites. These compounds delay the formation of tumors in mice by correcting the altered metabolic state of cancer cells, providing a potential therapeutic strategy for cancer treatment.
Scientists at Dana-Farber Cancer Institute have identified a new class of genes, dubbed CYCLOPS, that may serve as an Achilles' heel for many forms of cancer. These genes, which are essential to all cells but have been disrupted in cancer progression, can be targeted with drug molecules to block cancer cell proliferation.
Researchers propose targeting cancer cell communication to inspire new therapeutic approaches and potentially reactivate dormant cells. Cancer cells exhibit social behaviors like bacteria, including cooperation, task distribution, and immune evasion.
Researchers uncover chromosomal translocations that cause cancer, potentially leading to targeted therapies and personalized treatment. The study's findings may enable doctors to offer more accurate prognoses and inform treatment decisions.
Scientists have identified genetic alterations underlying a high-risk subtype of acute lymphoblastic leukemia (ALL) that can be effectively targeted with existing leukemia therapies. The study suggests patients with Ph-like ALL may benefit from the addition of imatinib and dasatinib to current chemotherapy regimens.
Researchers at Queen's University Belfast have discovered a new protein that plays a crucial role in regulating the spread of cancer cells. By targeting this protein, new therapies may be developed to prevent cancer from spreading.
Scientists are exploring ways to target cancer cells by attacking defective genes before protein production, leveraging micro RNAs (miRNAs) and their interactions with messenger RNAs. miR-7 and miR-128 affected pathways related to cell adhesion, EMT, and cellular replication in ovarian cancer cells.
Researchers have identified a new direction for cancer therapy by discovering a mutant form of the Chk1 gene that permanently stops cancer cell proliferation and causes cell death. This finding has the potential to reduce toxicity in cancer treatment, allowing physicians time to fix genetic errors.
A new study published in the FASEB Journal reveals that a molecule called 'flightless' significantly helps control cell movement through tissues. By increasing the stickiness of cells to underlying tissue, flightless slows their movement and may prevent cancer from spreading from one tissue to another.
A new biomarker, pyridoxal kinase (PDXK), has been identified as a predictor of response to chemotherapy in NSCLC patients. PDXK expression levels are associated with survival rates and treatment outcomes.
Researchers at Michigan Medicine have developed a safer method for steadying abnormal heart rhythms, using photodynamic therapy to target specific cells causing the arrhythmia. This cell-specific approach aims to decrease unwanted cell injury and inflammation, paving the way for more effective therapies.
Researchers found that paxillin regulates cell growth even in hormone therapy-resistant tumors, providing a new treatment target for advanced prostate cancer. The discovery could potentially lead to the development of targeted therapies that selectively attack cancer cells while leaving healthy cells intact.
Researchers at Arizona State University's Biodesign Institute developed the Cellarium, a live cell array technology that enables unprecedented insights into individual cell behavior. The system allows for dynamic measurements of live single cells, providing valuable clues to health and disease.
Researchers suggest using multicellular tumor spheroid (MCTS) models to improve cancer drug discovery, as they more accurately mimic human tumors. MCTS models can help identify specific genetic mutations targeted by drugs and interact with the surrounding environment.
Researchers at Moffitt Cancer Center found that inhibiting signal transducer and activator of transcription 3 (STAT3) can harness the immune system to eradicate residual malignant cells in drug-resistant mantle cell lymphoma. This strategy could provide a new approach for patients with therapy-resistant MCL.
Scientists at the Salk Institute have developed a protocol to convert cord blood cells into neuron-like cells, which may represent a new therapeutic option for neurological conditions. The method uses a single protein, Sox2, and demonstrates the conversion of cord blood cells into functional neurons.
A UCSF study reveals that a rare type of liver cancer may develop when one type of liver cell morphs into a totally different type, triggering tumors in mice. The discovery suggests that drugs targeting specific genes may provide a way to treat the deadly cancer.
Research established RNA Polymerase I (Pol I) activity as essential for cancer cell survival, and its inhibition with CX-5461 selectively activates p53 to kill tumors. The drug was shown to be 300 times more potent than non-genotoxic p53 activators.
A lipid, ceramide, helps cells find their way by keeping their antennae up, enabling direction and signal response. This function is crucial for maintaining proper cell locations, such as brain cells staying in the correct region.
A new strategy for treating aggressive skin cancer involves inducing cell differentiation to prevent tumor growth. Researchers identified a molecular mechanism that promotes the disappearance and inhibition of skin squamous cell carcinoma development.
Researchers have found that blocking a fundamental process deep within cancer cells can selectively kill them and spare normal cells. This discovery reveals that accelerated reading of ribosomal genes is responsible for causing abnormal nucleoli and is necessary for the survival of cancer cells.