Research on the cell biology of tumors. Covers cancer-cell vulnerabilities, tumor spread, nanoreactor therapies, and AI-guided cancer research.
A systematic review of seven studies found that low vitamin D levels are associated with an increased risk of bladder cancer. Vitamin D deficiency may be a key factor in preventing the cells within the bladder from stimulating an adequate immune response to abnormal cells, suggesting a potential mechanism for cancer prevention.
Pitt researchers discovered how oxidative stress accelerates telomere shortening by damaging DNA precursor molecules. This finding offers a new way to inhibit telomerase activity, potentially treating cancer. The study also reveals that oxidative stress can promote telomere lengthening.
A team of researchers discovered that immune T cells have two internal clocks controlling their lifespan and division, shedding new light on how the body regulates immune responses. The discovery also explains how errors in these clocks may lead to immune cell cancers such as leukaemia and lymphoma.
Researchers at the University of Georgia have discovered a drug combination that targets mitotic slippage, allowing for complete cell death and improving chemotherapy's effectiveness. The study focuses on inactivating CRL2-ZYG11, which promotes mitosis, and has potential to treat various cancers.
Researchers at Uppsala University developed a new approach to study cancer cells' reactions to treatments, enabling the identification of promising drug combinations. 3D tumor models mimic real-world conditions, where cancer cells have limited access to nutrients and oxygen.
Researchers discovered CD98 promotes AML, a type of aggressive cancer, and inhibiting it with the anti-CD98 antibody IGN523 blocks AML growth in patient-derived cells and mouse models.
Researchers found thousands of genetic translocations in both healthy and cancerous mouse cells, highlighting the importance of considering individual genetic backgrounds. By using 'de novo assembly', scientists can compare a patient's cancer cells to their own healthy cells, reducing errors in translocation discovery.
Researchers have broken down lung cancer into distinct subtypes with unique molecular profiles, suggesting potential for personalized therapies. The study identifies specific subsets of cancer cells that may be responsive to immunotherapy, a promising approach for treating the disease.
Researchers develop universal assay to detect cisplatin cross-linking sites in the genome. They found that mitochondrial DNA is a major target of cisplatin's action, while nuclear DNA is less affected.
Researchers use fission yeast to discover new cancer drugs targeting active proteins involved in DNA replication. The unique "arched and snapped" appearance of treated cells suggests potential for accelerating drug development.
Scientists at TUM have discovered new mechanisms of action for Imiquimod, a medication used to treat viral skin infections and certain types of skin cancer. The study reveals that Imiquimod activates the NLRP3 inflammasome, which can lead to inflammation and potentially contribute to its efficacy or adverse side effects.
A new treatment plan combining multiple targeted drugs for CML has the potential to increase life expectancy and reduce relapse risk. Mathematical modeling predicts optimal combination schedules based on tumor mutations, offering a personalized approach to cancer treatment.
Researchers found a way to break up p97 complex into its subunits using ASPL protein, which could be a promising new approach to kill proliferating cancer cells. This discovery may lead to the identification of smaller molecules that can disrupt the structure of p97 in a targeted manner.
Researchers identified amino acid valine as crucial for hematopoietic stem cell maintenance. A valine-free diet with gradual reintroduction led to successful long-term engraftment of healthy donor cells in mice.
Researchers used CRISPR to identify genes essential for AML cell survival, including the novel KAT2A gene. Inhibition of KAT2A destroys AML cells while sparing healthy blood cells in laboratory and mouse studies, offering new potential treatment options.
Researchers discovered that leukemia cells don't hide in specific niches but instead move actively throughout the bone marrow. This movement may help them survive treatment and evade targeted therapies.
Quiescent human cells exhibit an inflammatory profile similar to acute infections when energetically stressed, suggesting a pro-survival strategy may not be well-suited for long-term chronic stresses. This could impair genome repair and increase cancer risk.
Researchers will study cellular and molecular mechanisms of lung regeneration, targeting AT2 cells with gene editing techniques to correct disease-causing mutations and promote repair.
Researchers pinpoint a unique metabolic reprogramming in cancer cells that enables their ability to biosynthesize and replicate, and may provide new treatment opportunities. By blocking specific enzymes involved in this process, tumor growth can be slowed or stopped in preclinical tests.
Scientists at the University of Birmingham discovered a previously unknown mechanism connecting transcription machinery to genetic mutations in aggressive cancer cells. The research found that increased transcription activity leads to R-loop formation, causing DNA damage and replication stress.
Researchers at Johns Hopkins Medicine identified a protein that enables toxic alpha-synuclein aggregates to spread in the brain. A treatment strategy blocking this protein's action may slow Parkinson's disease progression, as antibodies already in clinical trials for cancer therapy show protective effects.
Researchers identified genes that control cellular senescence, a process that permanently arrests cell growth. These findings have potential applications for creating new anticancer drugs and developing anti-aging products.
Researchers discovered that certain proteins associated with Alzheimer's disease are stored in dormant cancer cells as amyloid bodies. Disaggregation of these bodies can reactivate the cancer cells. The study identified ribosomal intergenic noncoding RNA as a target for drug discovery to prevent amyloid body disaggregation.
Researchers have discovered a fluid behaving like water when trapped in a nanocage of a porous solid, offering new insights into nanoscale behavior. This breakthrough may lead to the design of machines with specific functions, including medical applications and molecular electronics.
Engineering researchers at the University of Texas at Austin have developed a new method for delivering chemotherapy directly and efficiently to individual cells using nanoparticles called 'connectosomes.' This approach has been shown to reduce the dose required to kill cancer cells by up to 10 times, potentially decreasing side effects.
Multiple myeloma cells communicate with healthy bone marrow cells, altering protein translation initiation to create a favorable environment for cancer growth. This crosstalk allows tumor cells to modify the surrounding microenvironment, promoting progression and disease.
Researchers at Johns Hopkins University School of Medicine have developed a new compound by attaching glucose to triptolide, making it more effective against cancer cells. The compound, glutriptolide 2, shows promise as a potential anticancer treatment with fewer side effects.
Researchers identified molecules controlling cell repulsion through endocytosis, a process by which cells engulf neighboring protein complexes. This discovery provides insight into development and neuronal networks, as well as cancer growth and metastasis.
Researchers have identified a specific signaling pathway in leukemia cells that enhances their viability and reproduction. The discovery highlights the potential for targeting this pathway to develop new treatments for acute lymphoblastic leukemia (T-ALL).
Tiny immune receptors on T-cells recognize antigens more effectively when clustered together, leading to improved immune response. This discovery could lead to new strategies to reprogram inactive T-cells and improve treatment for cancer and deadly infections.
Scientists have discovered a mechanism of intercellular communication that helps explain how biological systems function properly. The findings shed light on the poorly-understood interaction between cells and suggest that cancer cells' poor communication contributes to their biologic damage.
Researchers from Case Western Reserve University identified structurally abnormal genes in esophageal adenocarcinoma, which could serve as potential indicators of aggressive esophageal adenocarcinoma. The study found gene fusions that were highly associated with poorer patient survival and may aid tumor development.
Scientists at Johns Hopkins have discovered a drug combination that specifically targets the metabolic pathways of pancreatic cancer cells. By combining an experimental drug with metformin, researchers were able to shrink tumors by at least 50% in animal models, providing new evidence for treating this aggressive form of cancer.
Researchers created novel scaffolds with aligned ceramic nanofibers to control stem cell development and cancer cell behavior. The unique hybrid nano-network selectively guides stem cells towards specific lineages while suppressing inflammatory factors in cancer cells.
Fascin protein plays a crucial role in deforming the cell nucleus to navigate through tight spaces. The study suggests that this ability may be exploited by cancer cells to invade tissues, making fascin a potential target for therapy.
A new study by Queen Mary University of London found that certain Barrett's Oesophagus cells can be identified as 'born to be benign' or 'bad', allowing for early detection and prevention of oesophageal cancer. The test uses genetic analysis of individual cells, predicting future risk regardless of time since abnormal cell appearance.
Cancer cells counteract telomere breakdown by building them up with the enzyme telomerase. A new study using CRISPR gene editing technology reveals telomerase's mechanism, allowing scientists to identify potential targets for anti-cancer drugs.
Researchers at the University of Manchester have discovered a new test that can detect cancerous cells in the blood, offering a promising breakthrough in diagnosing and treating childhood leukemia. The test uses special structures called extracellular vesicles that are released by cancer cells and can be traced in the blood.
Researchers have developed a novel method to rapidly screen hundreds of chemicals for their anti-cancer properties by harnessing the power of knotted DNA structures. By detecting the activity of an enzyme crucial to cancer cell survival, this technique offers a promising tool for identifying potential new treatments.
Researchers at Thomas Jefferson University found that cold plasma can promote bone formation by enhancing cell/matrix attachments and increasing focal adhesion kinase activation. The study suggests that the technology could be used to improve bone healing in various medical applications.
Cancer cells use DR6 to kill endothelial cells, allowing them to slip through the vascular wall and form metastases. This process is known as necroptosis, which enables cancer cells to overcome an endothelial cell layer in the laboratory and in living organisms.
Pancreatic cancer cells use stellate cells to scavenge for energy, increasing mitochondrial metabolism and tumor cell growth. Alanine is the key fuel source that promotes tumor proliferation.
CNIO researchers identified a biochemical mechanism that enables cancer cells to survive without glucose, triggering a switch in proteins that control nutrient stress. This finding may help understand the resistance of cancer cells to anti-angiogenic agents and their ability to thrive in low-oxygen environments.
Researchers at Université de Genève have developed an antibody that blocks the migration of cancer cells, preventing their spread and proliferation. The 'H225' antibody reduces cancerous cell transit into organs by over 50% and limits cell proliferation, offering a promising new therapeutic strategy against lymphoma.
Researchers at the University of Copenhagen have developed a method that kills cancer cells using nanoparticles and lasers. The treatment has been tested on mice and shown to be effective in destroying cancer tumors without causing major side effects.
Cancer cells use oxygen gradients to navigate and spread through the body, according to a new study published in PNAS. Researchers at Johns Hopkins University found that cancer cells migrate from low-oxygen areas to higher oxygen concentrations, allowing them to reach blood vessels and metastasize.
Researchers at UC Berkeley have found a new cancer drug target that controls only a few percent of the body's proteins, potentially allowing for a more specific anti-cancer effect. The target is a protein called eIF3d that binds to specialized mRNAs and triggers translation of growth-promoting proteins.
Scientists at the University of Sussex are developing new cancer drugs that target DNA damage response pathways to selectively kill cancer cells. These drugs aim to maximize DNA damage or prevent its repair, leading to cancer cell death while minimizing harm to healthy tissues.
The study found treating colon cancer cells with a combination of curcumin and silymarin resulted in increased cell death and inhibition of cell multiplication. The researchers believe phytochemicals could provide an alternate therapeutic approach to cancer treatments.
Researchers have developed a new method to analyze scrambled cancer genomes, allowing for the simultaneous identification of two types of genetic changes and their connections. This tool, called Weaver, may help identify characteristics that distinguish cancers and inform personalized treatments.
Case Western Reserve University researchers identified why colorectal cancer cells depend on glutamine and developed a way to starve them. In a mouse model, exposing tumors with PIK3CA mutation to glutamine metabolism inhibitors suppressed tumor growth, providing a promising new therapeutic avenue for colorectal tumors.
Biophysicists at FAU discover that plastic cell deformation is caused by microscopic damage to the cytoskeleton. This finding helps characterize diseased cells more accurately, enabling better understanding of cancer, lung diseases, and heart diseases.
A new compound, mitoiron claw, protects skin cells from UVA-induced mitochondrial damage, preventing cell death and cancer. The researchers hope to see the compound added to sunscreens within 3-4 years.
Researchers at Caltech investigate the genetic switch that directs cells to become T cells, discovering a multi-tiered process involving four proteins that work together in three distinct steps. This finding has potential applications in boosting T-cell populations and fighting diseases such as AIDS.
Researchers at Duke University Medical Center discover that genetic mutations in pericyte cells lead to osteosarcoma and soft-tissue sarcoma. Activating beta catenin with lithium appears to limit cancer growth, offering new potential treatment options.
Researchers have identified a new class of molecules called selenocompounds that can kill multidrug-resistant cancer cells by blocking their defenses against chemotherapy drugs. The most active molecule worked almost four times better than the reference compound and induced cell suicide in cancer cells with similar potency.
A team of researchers from TUM has identified a molecular signaling pathway for programmed cell death that is suppressed in leukemia cells. This discovery offers new insights into the mechanisms underlying cancer progression and may lead to targeted treatment options.
Researchers found that mitochondrial stress triggers metabolic shifts through the p53 protein in cancer cells, leading to increased glycolysis and possible new targets for therapy. The study suggests that markers of metabolic stress could serve as a biomarker for cancer aggressiveness.
Researchers have identified NEAT1 as a key player in the survival of cancer cells, but its loss increases chemosensitivity and cell death. This discovery may lead to the development of new drugs targeting NEAT1 to enhance cancer treatment.
Researchers at UT Southwestern Medical Center have developed a new method to detect telomere length, which can influence cancer progression and aging. The new approach uses non-radioactive probes, increasing sensitivity and stability, and may help slow or stop cancer cell growth.