Research on the cell biology of tumors. Covers cancer-cell vulnerabilities, tumor spread, nanoreactor therapies, and AI-guided cancer research.
Researchers at Case Western Reserve University identified a way to increase the presence of the 53BP1 protein, which weakens cancer cells and makes them more susceptible to radiation and chemotherapy. The breakthrough could lead to improved cancer treatment outcomes if supported by animal model tests.
Researchers have found a new potential target for liver cancer treatment in the protein TREM-1, which accelerates chronic inflammation. Studies suggest that blocking TREM-1 can block the conversion of healthy cells to cancerous ones and even stop progression of existing cancer.
Researchers found that lung cancer cells sever protein ties, allowing them to break loose and spread. Targeting this process could stop lung cancer from spreading by keeping cells stuck together.
Penn researchers developed mathematical models of collagen matrix stiffness, providing insights into fibrosis, cirrhosis, and certain cancers. The models show that nonlinear elasticity can arise from the ECM's fibrous structure, allowing for long-range force transmission and bridging formation.
A study led by St. Jude Children's Research Hospital scientists has identified the population of white blood cells that tumors use to enhance growth and suppress the disease-fighting immune system. Monocytes are primarily responsible for T cell suppression around tumors.
Scientists develop novel class of molecules that could revolutionize immunotherapy for cancer and other diseases. The synthetic antibody mimics, or SyAMs, are smaller than current biologics and may avoid their risks.
A team of researchers has discovered a previously unknown form of multidrug resistance in cancer cells, known as inducible drug glucuronidation. By understanding this chemical pathway, scientists may be able to develop new treatments that can overcome this resistance and improve patient outcomes.
Researchers at Yale University have developed synthetic antibody mimics (SyAMs) that target disease cells and stimulate immune responses, offering potential for treating prostate cancer and other diseases.
Researchers found that infant cells must undergo a developmental process involving specific genes before they can participate in group interactions. The study identified the Lsd1 gene as crucial for ovarian follicle progenitor cells to mature at their normal rate.
Researchers found that adding thymine to normal cells stimulates gene production and causes them to multiply. This could lead to a treatment supplement to boost healthy cell production during chemotherapy, while minimizing side effects.
Researchers at the Buck Institute discovered that senescent cells secrete PDGF-AA, which accelerates wound closure and heals wounds normally. This finding suggests that cellular senescence may play a beneficial role in human health throughout the lifespan.
Researchers at the University of Manchester discovered a molecular 'tag team' controlling cell division in yeast cells. This relay system ensures proper regulation of mitotic exit, a critical step in preventing abnormal growth and cancer development.
Scientists at IRB Barcelona have identified two derivatives of borrelidin that completely remove the parasite load from mice and confer immunological memory to fight future infections. These compounds act on the protein production machinery of the parasite, making them efficient in all phases of infection.
Scientists at MCW found a link between sleep loss and cell injury, particularly in the liver, lung, and small intestine. Recovery sleep from deprivation restores balance and decreases cell injury, elucidating previous research on sleep abnormalities as risk factors for diseases like cardiovascular disease and cancer.
Researchers identified a critical pathway that enables cancer cells to survive despite DNA errors, relying on the PKCƐ signal pathway. Disrupting this pathway could trigger cancer cells to self-destruct, offering a new strategy to beat the disease.
In an early-phase clinical trial, a new type of cancer therapy targeting the IDH2 gene produced dramatic results in patients with advanced leukemia. The study found that AG-221 blocked the mutated protein, allowing immature white blood cells to develop normally and leading to complete or partial remissions.
New immunotherapy treatments aim to enable the body's natural defenses to recognize and destroy malignant cells. Studies present promising early data that encourage long-term outcomes among patients who have not responded to other therapies, including checkpoint inhibitors and drugs targeting the PD-1 pathway.
Researchers found that cancer cells and fibroblasts collaborate to invade the basement membrane, a process that begins long before the actual movement of cancer cells. CAFs secrete more proteases and matrix proteins than normal fibroblasts, which helps them remodel the basement membrane.
Researchers demonstrate that the innate immune system recognizes weaker cells and activates programmed cell death, eliminating them in a process called cell competition. This phenomenon has implications for cancer research and early disease detection.
Researchers at the University of Adelaide have discovered that cancer cells with chromosomal instability are vulnerable to mild metabolic disruption, making them a potential target for new therapy. The study's findings suggest that targeting these unstable cells could lead to more effective treatments with fewer side effects.
Researchers found high-dose interleukin-2 to be effective in metastatic renal cell cancer patients pre-treated with VEGF-targeted agents, achieving durable complete responses in a selected population. The therapy's efficacy and safety were confirmed, offering an alternative treatment option for carefully selected patients.
Researchers at MIT have developed a load driver device that can reduce unpredictability in biological circuits, allowing for robust and predictable behavior. This breakthrough could lead to applications such as biosensing and glucose monitoring for diabetic patients.
Researchers mapped p53 binding sites in human cancer and normal cells, finding the protein binds selectively to repeat sequences in cancer cells. This suggests p53's role in maintaining genomic stability and tumor suppression is context-dependent.
Researchers established induced pluripotent stem (iPS) cells from Werner syndrome fibroblasts, which can be used for drug discovery and gene therapy. The iPS cells have recovered telomeric abnormalities and similar expression levels of aging-related genes as normal iPS cells.
Research reveals Chlamydia trachomatis breaks down protective protein p53, allowing cells to mutate and develop into cancer. The bacterium exploits this mechanism to survive within host cells, posing a potential risk for cancer development.
Researchers have solved a decades-old mystery by uncovering the formation of massive DNA molecules, dubbed 'neochromosomes', in some tumours. These giant chromosomes are formed through catastrophic chromosomal shattering and genetic amplification, ensuring the cancer's survival.
Researchers have determined the structure of an ABC transporter complex, enabling targeted therapeutic approaches to combat antibiotic resistance and cancer cell defense. The study's breakthrough has significant implications for treating cystic fibrosis, bacterial infections, and cancer.
Researchers found a new strategy and potential drug to target faulty Ras protein, which causes cancer by producing excess signals. This breakthrough offers opportunities for developing new treatments that exploit the discovery without harming healthy cells.
Researchers have successfully triggered the self-destruct process in lung cancer cells, paving the way for a new treatment approach that leaves healthy cells unharmed. The breakthrough was achieved using a combination of two drugs, TRAIL and a CDK9 inhibitor, which altered the molecular switches in the cell suicide process.
Melbourne researchers have discovered the three-dimensional structure of a key cell death protein called Bak and revealed how it causes cell death. The study offers new targets for treating diseases such as lupus, cancers, and neurodegenerative disorders.
Two new studies from Johns Hopkins shed light on how complex cells detect and respond to minute differences in chemical concentrations. Cells use their internal 'skeleton' to influence gradient detection and movement, with implications for development, immune response, wound healing, and cancer metastasis.
Bio-engineers at ETH Zurich have created a biological circuit that controls sensor components using internal timers, enabling precise signal transmission. This breakthrough could lead to reprogramming cancer cells and creating complex bio-computers to detect and kill cancer cells.
The study identifies tiny differences in protein sequences between cancer cells and healthy tissue, enabling the creation of personalized vaccines. The research aims to improve treatment outcomes for patients with ovarian cancer, which often responds well to surgery and chemotherapy but returns lethally within a year or two.
A team of scientists has uncovered a new mechanism controlling actin-rich protrusions that aid in cell migration, a process essential for development, wound healing, and immunological responses. GMF protein plays a key role in regulating these protrusions.
Researchers at Imperial College London have developed a new cancer drug, DTP3, that selectively kills multiple myeloma cells without causing toxicity. The drug works by stopping the NF-kB pathway, which allows cancer cells to multiply, and has been awarded funding for clinical trials in patients with multiple myeloma.
Researchers at North Carolina State University have developed a DNA-based drug delivery system that targets cancer cells using nano-cocoons made of DNA. The system uses self-assembling DNA techniques and specifically delivers anticancer drugs to cancer cells, releasing them quickly once inside.
Researchers discovered that chromosome rearrangements can induce additional errors in cell division, leading to genetic instability. The study found that misplaced DNA segments can lead to the formation of extra cohesion sites, causing abnormal chromosome stretching during cell division.
Researchers found that nuclear factor kappa B (NF-kB) enables cancer cells to evade the immune system by suppressing genes that inhibit the immune response. Inhibiting NF-kB may make tumor cells more vulnerable to elimination by the immune system.
Researchers created a computer model that captures the exosomal exchange between cancer cells, dendritic cells, and other immune system cells. This new approach aims to find a better balance between cancer and the immune system, potentially leading to reduced side effects and improved treatment outcomes.
A $470,350 NSF award will support research on how proteins form groups or clusters within cells, which is associated with cancer and heart arrhythmias. The project aims to gain a better understanding of normal and abnormal protein grouping to prevent or correct abnormalities.
Researchers created a novel method for cell migration by mimicking the connective tissue environment, allowing cells to move in a controlled direction. This breakthrough could lead to new approaches in combating cancer metastasis and inflammation.
A new study reveals that individual cells' migration speed changes randomly through successive generations, despite the population's average speed remaining constant. This finding has significant implications for cancer treatment and tissue repair, suggesting a target for drugs to modulate cell migration speed.
Researchers have found that protein AIM can prevent liver cancer development by triggering the complement cascade to eliminate cancerous cells. AIM accumulates on the surface of HCC cells, leading to their destruction.
Researchers at the University of Missouri have discovered a molecule that effectively treats oxidative stress, which is linked to cancer, Alzheimer's, and Parkinson's disease. The compound, HPP-4382, has shown promise in fighting free radicals and could eventually be developed into a drug.
Phase II data showed dabrafenib has significant anti-tumour activity in patients with advanced BRAF V600E mutant non-small cell lung cancer. HER2 inhibition also shows promise in HER2-positive non-small cell lung cancer, with a 21% overall response rate in patients treated with neratinib and temsirolimus.
Researchers at the University of Missouri have discovered that a molecule used by bacteria can prevent cancer cells from spreading and even kill them. The 'stop spreading' bacteria molecule was found to stop multiplying, migrate, and begin dying in human pancreatic cancer cells.
Researchers have identified a better measure of predicting cancer neoepitopes, which are specific protein sequences recognized by immune cells. This new approach has the potential to improve current methods for generating anticancer vaccines, increasing their effectiveness in combating cancer.
A new technique uses perfluorocarbon tracers in combination with MRI to track therapeutic immune cells injected into patients with colorectal cancer. The study found that only half of the delivered cell vaccine remained at the inoculation site after 24 hours, but the technology shows promise for tracking other cell types and diseases.
Researchers at the Salk Institute have discovered a 'switch' in cells that can be turned on and off to control telomerase activity. This switch could help keep telomerase levels low, potentially slowing aging and regenerating vital organs.
The NIH has awarded over $64 million to six institutions to create a database of human cellular responses, known as the Library of Integrated Network-based Cellular Signatures (LINCS). This will improve scientists' understanding of cell pathways and aid in the development of new therapies for many diseases.
Ovarian cancer cells use mesothelial cells to spread through the body via fibronectin secretion. The study suggests that mesothelium is an active participant in the spread of ovarian cancer.
Researchers at Thomas Jefferson University have discovered a novel approach to killing colon cancer cells by using an antibody that targets the GUCY2C receptor, which is over-produced and exhibited on the surface of cancer cells. The immunotoxin selectively destroys colon cancer cells while sparing surrounding tissue.
A new cancer drug targeting mitochondrial function has been proven safe and showed some efficacy in a Phase I clinical trial for leukemia patients. The drug selectively shut down energy production in cancer cells, which can reproduce faster and repair damage from chemotherapy.
Researchers have developed an innovative algorithm that identifies synthetic lethal interactions in cancer, enabling personalized treatment and predicting patient prognosis. The study's findings show promise for repurposing existing drugs to target specific cancer types.
Yale Cancer Center researchers have found that lupus antibodies can selectively attack and kill cancer cells with defective DNA repair mechanisms. The study, led by James E. Hansen, suggests that harnessing these antibodies could be a new approach to targeted cancer therapy.
A new study confirms the role of invadopodia in cancer spread, showing that preventing their formation can stop cancer entirely. The study identifies a potential therapeutic target for drug development to prevent invadopodia formation.
Researchers have created an online analytic platform called CellNet to aid stem cell engineering. The tool uses network biology methods to analyze and predict cell fate and corresponding engineering strategies, offering a reliable shortcut for drug development and individualized cancer therapies.
Cells with oncogenic H-RAS activate ROS, which inactivates PTP1B, leading to AGO2 phosphorylation and gene silencing. This results in the accumulation of p21 proteins and halting the cell cycle.
Researchers at Virginia Commonwealth University Massey Cancer Center have developed a novel cancer therapy that leverages the autophagy defense mechanism to induce cell death in multiple myeloma cells. By targeting the p62 protein, the therapy disrupts autophagy and triggers apoptosis, resulting in increased effectiveness compared to t...
Researchers at Duke University have uncovered a 'roving detection system' on cell surfaces that may lead to new cancer therapies. The system involves receptors that search for signals to guide cell movement, potentially allowing for the prevention of metastasis and other diseases.