Research on the cell biology of tumors. Covers cancer-cell vulnerabilities, tumor spread, nanoreactor therapies, and AI-guided cancer research.
Researchers at Ohio State University found that the loss of microRNA-125b (miR-125b) shuts down normal cell metabolism and enables cancer cells to proliferate. The study reveals a new mechanism by which chronic lymphocytic leukemia (CLL) develops, providing potential targets for new drugs.
Researchers at WashU Medicine discovered that ACA11, a non-coding RNA, helps protect cancer cells from damage and makes them resistant to chemotherapy. This finding may lead to new cancer therapeutics and help guide research into better treatments for patients with multiple myeloma.
Researchers discovered that combining EGFR inhibitors with Wnt pathway inhibition can improve the durability of lung cancer remission. The Wnt pathway allows lung cancer cells to escape from EGFR-targeted therapy, but disrupting this pathway could lengthen the usefulness of existing treatments.
Researchers at UCLA found that glucose starvation activates a metabolic and signaling amplification loop that leads to cancer cell death. The discovery reveals the power of systems biology in uncovering relationships between metabolism and signaling.
Weill Cornell researchers devise innovative boxer-like strategy to deliver one-two punch to multiple myeloma by weakening defenses and then killing cancer cells. The approach, using two anti-cancer drugs, shows potential for treating other tumor types.
Researchers at Notre Dame have engineered nanoparticles that can target cancer cells in bone marrow, reducing the development of drug resistance and allowing for more effective treatment. The particles also reduce toxic side effects on healthy organs, promising a new approach to multiple myeloma therapy.
A study published in the Journal of Thoracic Oncology found that stereotactic ablative radiotherapy is an effective treatment option for elderly patients with stage I non-small cell lung cancer. The treatment did not negatively impact health-related quality of life, and functional and symptom outcomes remained stable after two years.
A new study at University of Illinois Chicago found that the enzyme AMP-activated protein kinase (AMPK) helps cancer cells survive during initial tumor formation and when they spread to other organs. AMPK promotes cell survival by regulating NADPH, a molecule that reduces harmful reactive-oxygen species.
A team at NIST has developed a method to calibrate and optimize color-based imaging techniques for medical applications. This enhancement enables surgeons to detect specific cell types with improved accuracy. The NIST effort is part of a larger initiative to evaluate and validate optical medical imaging devices.
A population of cells in the squamo-columnar junction of the cervix have been found to be responsible for most HPV-associated cervical cancers. These cells can become cancerous when infected with HPV, while other cells in the cervix appear to be resistant to infection.
Researchers at the University of Kentucky have developed two new ruthenium complexes that are up to 200 times more toxic and three times more potent than cisplatin against tumor cells. These complexes become activated when exposed to light, reducing their impact on healthy cells.
Researchers found that mitochondrial DNA mutations are lower in colon cancer cells than normal cells, contradicting previous beliefs. This discovery suggests that increasing mitochondrial DNA damage may lead to cancer cell death with minimal side effects.
A phase II clinical study shows that vismodegib can dramatically shrink basal cell skin cancers and prevent new ones in patients with basal cell nevus syndrome, a rare genetic condition. The treatment offers an alternative to surgical removal, but side effects remain a consideration.
Researchers have identified a prototype compound that can directly activate the BAX protein, leading to apoptosis in cancer cells. This new paradigm for designing cancer drugs may lead to new therapeutic strategies.
Studies show that ligand cells produce pulling force to pull on Notch, activating cellular responses. The findings provide compelling evidence for the role of mechanical force in Notch signaling, potentially leading to new therapeutic targets for diseases related to Notch signaling.
Researchers at Penn State have developed a biochip-based device that can rapidly screen cells for leukemia or HIV. The device uses microfluidic drifting technology to focus particles or cells in a single stream, eliminating the need for bulky lenses and mirrors, and potentially reducing costs to $1,000 from current prices of $100,000.
Researchers have found that cancer cells may require simpler genetic mutations than previously thought to grow and proliferate. The most common hemizygous deletions in cancer involve tumor suppressing genes called STOP genes, which are haploinsufficient, meaning they depend on two copies to function normally.
Researchers developed a stapled BIM BH3 peptide that competitively binds to anti-apoptotic proteins, leading to enhanced apoptosis in cancer cells. The compound suppresses tumor growth in mice and works synergistically with other pharmaceutical agents.
Scientists develop a technique to measure internal cell temperatures without altering cellular metabolism, opening doors for studying metastasis and differentiating healthy from cancerous cells. The 'fluorescence polarisation anisotropy' method uses green fluorescent proteins to provide non-invasive temperature readings.
Researchers at Stanford University have developed a method to repeatedly encode, store and erase digital data within the DNA of living cells. This breakthrough enables the creation of a binary digit equivalent to a 'bit' in data parlance.
A new study describes a compound that selectively kills cancer cells by restoring the structure and function of mutant p53. This finding supports the development of rationally targeted cancer therapies and has potential for treating 30,000 patients annually in the US.
A Mayo Clinic study has found that exhaustion affects immune cells fighting cancer, rendering them less effective. The research suggests a new approach to lymphoma and other cancers by dampening cell-signaling molecules like IL-12.
Two UC Davis faculty members, Frederic Chedin and Noriko Satake, received Individual Biomedical Research Awards to explore novel approaches to understanding autoimmune diseases. Paula Goines, a postdoctoral researcher, will also receive funding for her work on autism research using nerve cells grown from adult stem cells.
The University of California, Santa Cruz, has established the Cancer Genomics Hub to manage and analyze large-scale cancer genomic data. This hub will support research programs like The Cancer Genome Atlas and enable personalized cancer care by connecting specific genomic changes with clinical outcomes.
Researchers have made a groundbreaking observation of cellular architecture using high-powered microscopes, revealing the structure of microtubules during gamete formation. The findings could impact the treatment of diseases caused by misregulation of microtubule structures, including Down syndrome and cancer.
Researchers have created a new instrument that rapidly analyzes the physical properties of cells to identify cancer and other cell states. The deformability cytometer measures cells' responses to fluid flow, providing valuable information about cell health.
Researchers have identified a second form of the MCL1 protein, which works in a different location and performs a different function. The newly discovered version is shorter and located inside mitochondria, where it promotes mitochondrial energy production and may aid in cancer treatment.
Researchers have found that adding boron-nitride nanotubes to cancer cells can increase the effectiveness of a minimally invasive treatment for soft tissue tumors. The treatment, known as Irreversible Electroporation, has been shown to kill twice as many cancer cells when BNNTs are present on the cell surface.
Researchers at Simon Fraser University found that cholesterol-binding proteins called ORPs can control cell growth, potentially slowing down cancer cells. Genetic changes blocked the ability of these proteins to bind cholesterol, but altered ORPs actually stimulated cell growth by activating regulator proteins.
Researchers at Huntsman Cancer Institute have discovered that normal epithelium tissue ejects living cells to maintain a steady population and ease overcrowding. This mechanism is crucial in preventing cancer, as it allows cells to turnover and prevents cell pile-ups, which are common in cancerous tissues.
Researchers create iPhage particles that penetrate cells using penetratin, targeting specific organelles like mitochondria and ribosomes. They discover a peptide ligand that disrupts ribosomal function, killing cancer cells and reducing cell survival in malignant and non-malignant cells.
Researchers develop new methods for injecting drugs and genetic payloads directly into cancer cells using plasmonic nanobubbles. Delivering chemotherapy with nanobubbles increases efficacy and reduces dosage, targeting single-cell level cancer treatment.
Researchers identified a novel anti-leukemia compound, Lenaldekar, that demonstrates effectiveness in eliminating immature zebrafish T-cells and targeting human T-ALL cell lines. The compound showed promise in treating cells from patients with other leukemias, including those resistant to current therapies.
Researchers discovered that the Nrf2 protein plays a crucial role in protecting cells from oxidative stress, which is often exploited by cancer cells to become resistant to treatment. By selectively inhibiting Nrf2, cancer cells may become more susceptible to chemotherapy and radiation therapy.
Researchers found EPR to be 30-46% better at identifying nonmelanoma skin cancer cases compared to claims data. The study suggests using EPR as an alternative for effectively tracking these cases, potentially improving disease burden estimates.
Researchers propose that non-genetic resistance can occur before genetic mutations, changing the approach to designing combination therapies. This new perspective aims to improve outcomes by understanding how cancers evolve and adapt to extreme challenges.
A new drug developed by Northwestern Medicine scientists has prevented human prostate cancer cells from spreading to other tissues. The drug inhibits movement of the cells and prevents metastasis without causing harm to normal cells or tissues.
Scientists have identified PRC2, a chromatin regulator, as a promising therapeutic target in acute myeloid leukemia. Blocking PRC2 halts uncontrolled proliferation and reactivates anti-tumor pathways, offering a potential new treatment option.
Scientists will investigate the role of Myc oncoproteins and a specific mRNA-binding protein, TTP, in controlling tumor growth. The study aims to define mechanisms that could lead to the development of new anti-cancer drugs.
New cell printing technology enables precise pattern formation of human cells, paving the way for advancement in tissue engineering and regeneration. Researchers demonstrated the use of acoustic droplet ejection followed by aqueous two-phase exclusion patterning to control cell placement.
Researchers propose that quantum metabolism explains metabolic changes causing healthy cells to become cancerous, enabling cells to outcompete for space and nutrients. Understanding this process could lead to new cancer treatment approaches.
Researchers developed a new pulsed photoacoustic technique to detect a small number of cancer cells in vitro. The technique combines high optical contrast with high resolution, allowing for the detection of single cancer cells.
Researchers at Queen Mary University of London have identified a mechanism by which normal cells can become cancerous. By understanding how the FOXM1 gene influences cell behavior, scientists may be able to develop new diagnostic tests to detect cancer at an early stage.
Researchers have discovered that a specific protein called p21 can kill certain cancer cells, including sarcomas, by sensitizing their mitochondria to oxidants. This finding provides a rationale for testing existing drugs that increase p21 levels in these types of cancers.
Researchers aim to create targeted compounds that selectively attack cancerous cells by zeroing-in on pollutants produced by tumors' characteristic metabolism. This approach seeks to minimize side effects associated with conventional chemotherapy.
Researchers discovered a two-step ritual in which RNA telomerase partners are prepared for interaction, revealing novel pharmaceutical approaches to cancer and diseases of aging. The study sheds light on the complex process of telomerase biogenesis and its connection to seemingly unrelated diseases.
Researchers at Stanford University have directly observed plasmon resonances in individual metal particles measuring down to one nanometer in diameter. This discovery could lead to advancements in catalytic processes, cancer research and treatment, and quantum computing.
Researchers say forcing dying cancer cells to trigger an immune response could prevent cancer relapses and improve treatment benefits. The new strategy focuses on autophagy, a process that alerts the immune system to foreign invaders.
Researchers found that adding RNAi to standard TKI or antibody therapy can enhance the effect of therapy on NSCLC cell death and slow cell growth. The treatment may benefit patients with EGFR mutations who do not respond to TKI, or those whose cancer is driven by overactive EGFR production.
Researchers at Sanford-Burnham Medical Research Institute found that MLN4924-resistant cancer cells escape death due to a simple mutation in the NEDD8-activating enzyme. The team developed a method to predict how cancer patients will respond to this drug, providing a new path toward personalized medicine.
Scientists have successfully mapped tens of thousands of molecular signaling events involved in DNA damage repair, shedding light on how cells communicate when their DNA is broken. This research will help develop new drugs with fewer side effects and better protect healthy cells during cancer treatment.
Researchers sequenced DNA from cancer cells in patients with myelodysplastic syndromes who later developed leukemia, finding that the disease is an early form of cancer. The study suggests that targeted cancer drugs should be aimed at mutations that develop early in the disease.
Researchers at RIKEN successfully developed a new experimental technique for producing cells with specific functions by reconstructing transcriptional regulatory networks. This technique enables faster and more efficient production of functional cells for cancer therapy and other applications.
A recent study found that the protein Mer resides in the nucleus of leukemia cells, suggesting it may influence gene expression and contribute to cancer development. This discovery opens up new avenues for targeted treatments and potentially more accurate diagnoses.
A major study published in the Journal of Clinical Investigation has identified a method to stop bladder cancer from metastasizing to the lungs. The study found that adding the protein RhoGDI2 to tumors reduces versican production, blocking the ability of cancer cells to grow in the lungs.
Researchers found that telomeres send out a molecular SOS signal when cells take too long to divide, leading to the activation of DNA damage pathways and cell death. This discovery has implications for cancer chemotherapy, suggesting ways to make therapy more potent by combining mitotic inhibitors with other drugs.
Researchers at Weill Cornell Medical College have developed a new tool to image small-molecule metabolites in living cells, offering clues about how to treat disorders. The technology uses modified RNA called 'Spinach' to sense levels of target metabolites in real-time.
Cancer cells use an 'emergency brake' to protect themselves from chemotherapy drugs, which can be rendered inoperative by targeting a specific enzyme pathway. The study identifies PARP inhibition as a promising therapeutic approach to improve chemotherapy effectiveness.
Researchers found that a protein called FOXM1 protects cancer cells from chemotherapy and radiation-induced cell death. Combining standard drugs with proteasome inhibitors may improve treatment effectiveness.
A team from UNC Chapel Hill discovered how a long-studied protein complex influences cell movement and how cells respond to external cues. Cells without the protein complex exhibit altered structure and movement, affecting their ability to sense chemical cues and navigate surfaces.