Research on the cell biology of tumors. Covers cancer-cell vulnerabilities, tumor spread, nanoreactor therapies, and AI-guided cancer research.
Researchers at Vanderbilt University Medical Center discovered that the Golgi apparatus is a novel source of microtubules in cells, which are crucial for cell movement and division. This finding could lead to new insights into cancer cell invasion and treatment strategies.
Researchers at Louisiana State University studied the effects of gold-based nanoparticles on cell freezing, which could impact cancer treatment. Despite initial expectations, the study found significant damaging interaction between nanoparticles and cancer cells.
Researchers have successfully observed cell migration in real-time using a specialized liquid culture medium, shedding light on the nuances of organized cell movement. This breakthrough could lead to strategies for regulating both normal growth and cancer progression.
GSK has launched a Phase III trial evaluating its novel immunotherapy MAGE-A3 ASCI in patients with stage IB or II NSCLC. The trial aims to assess the efficacy and safety of MAGE-A3 ASCI as adjuvant therapy following surgery.
Researchers at St. Jude Children's Research Hospital discovered that cancer cells can increase GAPDH production to counteract the backup self-destruct program CICD, allowing them to survive and thrive. The finding suggests that blocking this enzyme could kill abnormal cells, providing a basis for novel anti-cancer drugs.
Researchers found that the p53 gene activates microRNA miR-34a, which kills cells with damaged genes. This microRNA plays a crucial role in stopping tumor development and is often missing in pancreatic cancer cells.
A study at the University of Pittsburgh School of Medicine found that green tea's catechins protected normal and cancerous bladder cells from inflammation. The findings suggest herbal supplements from green tea could be a treatment option for various bladder conditions.
Two UI studies show that the NSAID celecoxib has potent anticancer activity, killing head and neck cancer cells in the S phase of the cell cycle. This finding suggests that combining celecoxib with chemotherapies may provide better tumor control than radiation alone.
Research suggests that TRPM8 is overexpressed in prostate cancer cells, indicating its potential as a therapeutic target. The study also found that endoplasmic reticulum TRPM8 retains functional activity regardless of cell differentiation status, which may contribute to cancer cell growth.
Researchers created a dynamic model to understand cellular signaling pathways in C. elegans, revealing gaps in current understanding and potential for future exploration of biological systems. The model can predict how cells respond to gene mutations and signals, saving laboratory time and resources.
Researchers found that FDG-PET imaging can identify patients who respond to chemotherapy, allowing for early termination of futile treatment. This improves patient care by providing an alternative approach, such as stopping chemotherapy or switching to a more adequate therapeutic option.
Researchers identified a genetic mechanism that permanently shuts down crucial genes in healthy immune system cells, which could be used to target cancer and infection treatments. The discovery was made in normal blood samples and found in a quarter of leukemia samples, highlighting the potential for this mutation as a therapeutic target.
Researchers have developed a method to analyze the entire network of signaling proteins controlling cell movement. The study provides the first comprehensive profile of these proteins, shedding light on the inner workings of the 'steering wheel' that drives cells forward.
Researchers at Johns Hopkins found that cancer cells can reprogram themselves to use less oxygen and more glucose, allowing them to survive and spread. The loss of a single gene causes cancer cells to stop making mitochondria, leading to the use of fermentation for energy production.
UK pharmaceutical sciences graduate student Abby Ho and assistant professors Kyung-Bo Kim and Royce Mohan developed a new compound dubbed UK-101 that acts directly on LMP2, a component of the immune proteasome variant abundantly expressed in certain tumors. The researchers found that UK-101 inhibits LMP2 while not attacking normal cell...
A Johns Hopkins team has discovered that shortening chromosome ends, called telomeres, can prevent cancer cells from growing by inducing a process known as senescence. This breakthrough could lead to new ways of preventing or treating cancer.
A new study suggests that targeting the survival protein Mcl1 may be an effective way to treat leukemia, particularly when combined with existing drugs like rituximab. The research found that knocking out Mcl1 can cause cancer cells to die, and combining it with rituximab killed significantly more leukemia cells than the drug alone.
A mouse model has been developed to study the relationship between hypoxia and cancer progression in renal cell cancer. The researchers observed that Fh1-deficient mice developed clonal and proliferative renal cysts with characteristic overexpression of HIF, leading to renal failure.
Researchers are investigating a genetically modified variant of Avian Newcastle disease virus to treat human prostate cancer. The virus is designed to replicate only in the presence of prostate-specific antigen, found exclusively in cancerous cells.
Researchers at Samuel Lunenfeld Research Institute have discovered a connection between sugar modifications on proteins and cancer. The study shows how these modifications control protein availability, affecting cell behavior and tumor growth.
Karl Scheidt and his team have synthesized 10 different flavanones, a type of flavonoid, using a new general method that takes advantage of one simple catalyst. The findings provide a method for making new molecules based on flavonoids, setting the stage for the development of new cancer therapeutics.
Researchers at the University of Pennsylvania School of Medicine have demonstrated that injured pancreatic cells readily regenerate back into healthy acinar cells. This finding holds promise for treating cancer and inflammation of the pancreas, while shifting focus from regenerating insulin-producing beta cells.
A recent study found that reducing calorie intake later in life can induce health and longevity benefits similar to lifelong calorie reduction. The researchers discovered that certain drugs mimic this effect, which may lead to the development of new
Scientists discovered a protein that enables cells to bypass damaged DNA during replication, averting cell suicide. However, this protein also makes errors that may contribute to the development of cancer.
A new procedure, anal cytology, detected abnormal cell changes in 244 HIV-positive patients, leading to subsequent biopsy confirmations. Abnormal results prompt further investigation and management.
Scientists at Dana-Farber Cancer Institute mapped the structures of small molecules and mutated protein receptors in non-small cell lung cancer cells. They found that two inhibitors bind more tightly to specific mutations, potentially leading to more effective treatments.
A study published in Cancer Cell reveals that a specific sequence of genetic mutations determines the behavior of cystic pancreatic cancer, which has a 50% long-term survival rate. The research found that cells with this mutation are resistant to TGFb's tumor-promoting properties, contributing to their improved survival.
Researchers found that vitamin A derivative ATRA increases levels of miRNA-15b and miRNA-16-1, which inhibit Bcl-2 gene activity. This helps explain how the drug works by regulating genes that need to be silenced for cell differentiation.
Researchers identified 50 genes that interfere with genetic activities of genes causing uncontrolled cell division. These genes work by producing proteins that directly attach to cell-division genes, hindering their activity.
Research by Cold Spring Harbor Laboratory finds that harmless viruses can cause cancer through chromosomal instability, potentially leading to cancer progression. Protecting against these viruses may decrease cancer incidence.
Researchers used a microfluidic chip to study the mating habits of yeast cells, revealing that a second MAPK plays a crucial role in the process. The findings shed new light on how cells send and receive signals from one another and from their environment.
Researchers identified a new route to cancer treatment by exploiting mutations that control cell movement. Understanding the collaboration between Ras and p53 genes may lead to novel therapeutic targets like Rho proteins.
Robert C. von Borstel presents cancer as an invasive process similar to species evolution, with mutations and selection driving its progression. He hopes his work will help people re-examine cancer in a new light.
Researchers at TRIUMF are developing custom radioisotopes to target cancer cells more efficiently. They aim to create tailor-made treatment programs for each patient, reducing radiation doses and treatment sessions.
Researchers have found a way to deliver a messenger into cancer cells that forces them to respond to death signals using an HIV protein. This approach has shown promise in killing cancer cells and could provide new treatment options for patients with deadly cancers.
A new study finds that p38-alpha MAPK inhibits tumor formation by sensing oxidative stress and triggering apoptosis. Cancer cells may evade this mechanism by desensitizing p38-alpha to ROS, highlighting potential therapeutic targets for cancer treatment.
A new medical technique using microsecond electrical pulses has been shown to create permanent nanoscale holes in target cell membranes without harming surrounding tissue. This technique, called irreversible electroporation (IRE), has the potential to revolutionize minimally invasive surgical treatments for tumors.
Purdue University researchers use dendrimers to label specific proteins in living cells, allowing them to determine protein functions and diagnose diseases. This new method provides a more reliable alternative to existing methods, which require small sample amounts and damage the natural environment.
Researchers developed a small-molecule inhibitor of Plk1, a key kinase controlling cell division. The compound BI 2536 effectively halts cancerous cell growth in culture and in animal models, causing cell death and tumor regression. This discovery has therapeutic potential for patients with locally advanced or metastatic cancers.
Researchers at Oncolytics Biotech have developed a harmless virus that not only kills tumor cells but also primes the immune system to mount a powerful defense against cancer. Studies have shown that reovirus exposure can activate dendritic cells, which then educate natural killer cells and T cells to attack the tumor.
Researchers at Brown University have identified GABP as a critical transcription factor that restarts cell division, a process fundamental to development, renewal, and cancer growth. Disrupting GABP may lead to new cancer treatments.
Scientists have linked telomere loss to both cancer and aging by visualizing chromosomes of cells from patients with Werner Syndrome. Rebuilding structures called telomeres significantly blocks genetic damage seen in cells of patients with Werner Syndrome.
Researchers discovered that ceramide helps stem cells organize into primitive ectoderm, which further differentiates into embryo tissues. The lipid's presence is essential for cell polarity and differentiation.
Researchers at University of California, San Diego found a molecular link between chronic inflammation and cancer development. The protein p100 enables communication between inflammatory response and normal cell growth, but excessive levels may overactivate developmental pathways, leading to cancer.
A new strategy for fighting cancer aims to make its genes get lost in translation, silencing oncogenes by targeting weak messenger RNAs. The researchers discovered a small molecule that effectively inhibits the translation of these weak mRNAs, leading to the decline of cancer-promoting proteins.
A new test developed by Dana-Farber Cancer Institute scientists identifies malignant blood cells that are highly vulnerable to an experimental cancer drug. The drug works by neutralizing the Bcl-2 action, unleashing molecules that trigger suicide in the cancer cells.
Researchers have made a breakthrough in molecular technology that could help deliver life-saving drugs directly to cancer-ridden cells. The discovery involves attaching therapeutic drugs to molecules using tiny molecules that can travel through the bloodstream.
Researchers at Rice University have developed a novel way to deliver drugs directly into cancer cells using buckyball nanoparticles as passkeys. The technique, which mimics viral proteins, shows promise in penetrating the defenses of liver and neuroblastoma cancer cells, two types often difficult to treat.
Researchers found that the p53 gene's ability to direct a damaged cell to stop growing or commit suicide depends on turning on separate groups of target genes. Alterations in an amino acid, lysine 120, can influence this decision, potentially leading to new strategies in chemotherapy drug development.
Researchers at Johns Hopkins University have developed a hybrid molecule that combines a sugar with a short-chain fatty acid to kill cancer cells in lab tests. The molecule triggers cellular suicide and orchestrates the expression of genes responsible for halting uncontrolled growth.
The study found that AVN944 significantly inhibited the IMPDH enzyme and induced biomarkers associated with cancer cell death. The gene HspA1A marker was elevated even at low doses of the drug, indicating potential for tumor cell apoptosis.
Scientists discovered that higher body mass, not lifespan, increases the risk of cancer due to telomerase expression. Rodents from various species showed a correlation between body size and telomerase activity, while human's don't express it in somatic cells, suggesting evolution prioritized cancer prevention over healing.
A new technology allows users to record and store massive amounts of data onto a single disc, such as the Smithsonian National Air and Space Museum's entire collection or 500 movies, maintaining excellent quality without damage. The UCF team's Two-Photon 3-D Optical Data Storage system uses lasers to compact information onto a DVD.
Researchers at Children's Hospital Oakland Research Institute identified a specific enzyme called sphingosine phosphate lyase (SPL) that can cause the death of cancer cells. The study found that SPL makes cancer cells more vulnerable to chemotherapy, while removing the enzyme makes the cells more resistant to treatment.
Researchers at the Salk Institute reveal how cellular repair proteins recruit a second machinery to create a protective structure at chromosome ends, maintaining chromosomal stability. Telomeres exist to prevent damage and ensure cell division integrity.
Researchers suggest repairing abnormal blood vessels in retinopathy using adult bone marrow–derived myeloid progenitor cells. Dendritic cells form part of granuloma walls containing Listeria monocytogenes, maintaining integrity through immunosuppressive protein IDO.
ABT-737, a BH3 mimetic, targets Bcl-2 proteins to induce apoptosis in cancer cells. The treatment has shown effectiveness against acute myeloid leukemia (AML) cells and can be combined with MCL-1 inhibitors for improved results.
The ACE experiment found that antiprotons are four times more effective at terminating live cells than protons, with the potential to reduce damage to healthy tissue. Researchers plan further tests to assess the effectiveness of antiprotons for cancer therapy and ensure minimal harm to surrounding tissues.
Researchers found that white blood cells in cancer-resistant mice can sense and kill cancer cells through a multi-step process, involving migration, recognition, and physical contact. The discovery suggests that some cancers may share common characteristics that make them vulnerable to this type of immune response.
Researchers at Max Planck Institute for Molecular Genetics in Berlin have explained the molecular principles of cell division control mechanisms. The study found that checkpoint kinases interact with a different category of proteins involved in developing the cell division spindle.