Articles tagged with Tumor Cells
Researchers found that detecting poorly differentiated basal tumor cells in early-stage cancers and overexpressing cell division cycle 25C can predict an increased risk of death. A test for this protein could help determine whether a patient is likely to benefit from drug treatment.
Researchers have discovered that SLC6A14 is overexpressed in pancreatic tumors and cancerous cells, transporting amino acids for cellular metabolism. Blocking SLC6A14 with alpha-methyltryptophan starves pancreatic cancer cells, reducing growth and proliferation
Tumor cells attract macrophages by releasing cytokines, which secrete growth factors that help tumor cells form spheroids and grow. Inhibiting these growth factors reduces tumor cell proliferation in a mouse model of ovarian cancer. This study sheds light on the early stages of ovarian tumor metastasis.
Researchers at Sanford Burnham Prebys Medical Discovery Institute found that a key signaling protein helps suppress inflammation and scarring in the liver. The study suggests that p62, which is usually absent from cells that initiate inflammatory signals, plays a crucial role in preventing liver cancer progression.
The CheckMate 026 trial found that nivolumab did not improve progression-free survival over chemotherapy in patients with PD-L1 positive tumours. However, combination immunotherapies are being investigated to potentially increase the proportion of patients who benefit from treatment.
Researchers found that platelet α6β1 integrin promotes interactions between tumor cells and platelets, leading to decreased lung metastasis in mice. Antibody-mediated blockade of α6β1 integrin inhibited tumor metastasis in murine models of breast cancer and melanoma.
Researchers at IDIBELL discovered that tumor microenvironment triggers processes to protect tumor cells from conventional chemotherapy. The presence of certain molecules slows down cell cycle and activates proteins minimizing treatment effectiveness.
Researchers developed an assay to identify chemotherapy-resistant cells in acute myeloid leukemia (AML) tumors. The least sensitive cells can predict a patient's response to chemotherapy, improving therapeutic outcomes.
Scientists have discovered unique genome variants linked to cancer development, which can be used to detect weaknesses in tumor cells. The new approach uses proteogenomics and mass spectrometry data to identify variant peptides, providing valuable information for gene annotation and potential drug targets.
Researchers found that esophageal cancer cells do not divide faster than their normal neighbors, but instead produce slightly more dividing daughter cells. This imbalance in cell division can lead to tumor growth over time, making it harder to treat with current therapies.
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.
This study explores the structural features of quercetin derivatives that inhibit EGFR protein in NSCLC cells. The researchers developed a pharmacophore model that identified key features, such as hydrogen bond acceptors and aromatic rings, which are associated with effective inhibition.
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.
Scientists at The Wistar Institute identified a critical pathway driving tumor adaptation in hypoxic conditions, enabling tumor cells to survive and proliferate despite low oxygen levels. This pathway, involving the protein Akt and PDK1, has implications for glioma treatment and potential therapeutic targets.
Researchers have identified a marker for myeloid-derived suppressor cells (MDSCs) that distinguish them from normal neutrophils. Higher numbers of these cells are associated with larger tumor sizes, suggesting the marker could help predict disease severity and outcome.
Three Syracuse University physicists are using a $686,000 NSF grant to study the dynamics and interactions of cancer cells and develop a better understanding of tumor behavior. Their research aims to shed light on tissue behavior, cell segregation, and cell escape.
Case Western Reserve University researchers uncover key surface proteins in brain tumors that allow them to evade the immune system. The study found that blocking protein Cdk5 enables CD4+ T cells to remove tumor cells, suggesting a potential new therapy for brain cancer.
Researchers designed an engineered protein to repress a specific cancer-promoting message within cells, paving the way for precise treatments with fewer side effects. The protein, Rbfox2, was modified to bind to microRNA miR-21, which is present in high levels in many tumors.
Researchers identify CD47 protein in atherosclerotic plaques, which enables immune system to evade clearing dead cells, leading to plaque buildup and cardiovascular disease. Anti-CD47 antibodies show promise in preventing plaque formation and regression in mouse models.
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 at Hokkaido University found that biglycan molecule attracts tumor cells to blood vessel walls, facilitating metastasis formation. High biglycan expression linked to poor prognosis in breast, lung, and colorectal cancer patients.
Researchers at MUSC discovered that Dab2 is a molecular switch regulating autophagy or apoptosis in tumor cells. Maintaining Dab2 levels blocks autophagy and promotes cell death, enhancing chemotherapeutic agent efficacy. In vivo studies showed Dab2 reduces tumor metastasis and increases drug-induced cell death.
Researchers have identified the 'cell of origin' in basal cell carcinoma, a common form of skin cancer, as stem cells. By analyzing clones derived from mutant stem cells, they found that these cells can overcome apoptosis and divide unchecked, leading to cancer growth.
Researchers at The Wistar Institute have discovered a specific network of proteins present in the mitochondria of cancer cells that enables their ability to proliferate, migrate, and spread. By targeting this pathway, they believe it may be possible to develop new treatments for various types of tumors
Researchers at Osaka University discovered that a group of T-cells with low FOXP3 expression, known as FOXP3-low T cells, facilitate cancer immunity in colorectal cancers. These findings suggest new potentials for treating CRCs via regulation of intestinal bacteria and defining patient groups. Intestinal bacteria induce inflammation in...
Researchers at H. Lee Moffitt Cancer Center & Research Institute used a mathematical model to show that tumor cells on the edge and interior develop distinct characteristics, investing resources in survival or invasion, respectively.
Researchers discover new function of STAT1 in activating natural killer cells to eliminate tumor cells. Without this newly identified function, NK cells are still effective in eliminating tumors.
Researchers at TUM identified the molecular mechanism of thalidomide, revealing a common link between its teratogenic and anti-cancer effects. The study found that disrupting the protein complex CD147-MCT1 leads to both developmental defects and tumor cell death.
Researchers found that combining radiotherapy with PD-1 blockade therapy improved survival rates in a murine lung cancer model. However, this treatment approach showed no benefits for tumors that had relapsed after radiation therapy, highlighting the need for personalized medicine strategies.
A new laboratory test developed by Johns Hopkins Medicine accurately clocks the 'speed' of human brain tumor cell movement, which may predict how quickly and aggressively a given cancer might lethally spread. The assay has been tested on 14 glioblastoma patients and showed promising results in predicting clinical outcomes.
Researchers developed a new compound to target mutated p53 genes, found in over 50% of cancers, which are responsible for uncontrolled cell growth. The treatment has shown promising results in patients with modest toxicity, and trials will now expand to 400 patients across Europe and the USA.
Researchers identified key metabolic pathways altered in prostate cancer, with a potential therapeutic target for castration-resistant prostate cancer. Studying tumor metabolism offers new possibilities for treatment.
Walter and Eliza Hall Institute researchers have identified a protein 'brake' that controls Natural Killer cell activity, revealing a potential therapeutic target. The study showed that removing this brake improves Natural Killer cells' ability to fight metastatic melanoma, offering hope for new immunotherapies.
A recent study by Johns Hopkins Kimmel Cancer Center scientists reveals that the HOXA5 protein plays a crucial role in maintaining normal breast cells' traits, such as adhesion and cell plasticity. The loss of HOXA5 leads to increased tumor aggressiveness and poorer outcomes for patients.
Cancer cells use notch signaling pathways, particularly jagged, to communicate and coordinate their decisions to become motile and form clusters. This discovery offers a new target for disrupting metastasis and potentially diagnosing tumor severity.
A new cancer immunotherapy approach combines the power of tumor-fighting immune cells with fewer side effects. By converting T regulatory (Treg) cells into T effector (Teff) cells, this method targets tumors while protecting healthy tissues.
Researchers have discovered a tollerance mechanism in NK cells that restrains their ability to kill cancer cells. Increasing IL-15 levels may improve immune responses against tumors.
Researchers at the University of Chicago found that inhibiting autophagy, a cellular housekeeping process, effectively blocks tumor cell migration and breast cancer metastasis in tumor models. Autophagy is essential for tumor metastasis, and its inhibition can be an effective approach to block metastatic dissemination.
Researchers develop an experimental therapy that shuts down the Olig2 gene, halting tumor growth and blocking tumor formation. The approach uses a gene therapy to eliminate Olig2-positive cells, sensitizing them to targeted molecular treatment.
Researchers at Duke University Medical Center have developed an antibody that selectively attacks cancer cells while sparing healthy ones. The antibody works by targeting a specific protein on cancer cells, disabling their defense mechanism and triggering an immune response.
A recent study at The Hormel Institute has uncovered a new molecular mechanism that detects missegregated chromosomes and prevents the formation of tumors. This discovery provides insight into the regulation of chromosome segregation and its role in cancer development.
Tumor cells switch to glycolysis, a form of anaerobic energy production, allowing them to continue growing even without new blood vessels. This discovery opens up new possibilities for long-term cancer treatments by inhibiting anaerobic energy production or transport of lactic acid.
Cancer cells' ability to slide past obstacles and travel out of primary tumors is enabled by abnormal protein fiber scaffolding and the agility of cancer cells themselves. The researchers developed a model environment that mimics protein fibers, allowing them to observe and quantify the behavior of breast cancer cells.
A new University of Illinois study reveals that the shape of a tumor may play a significant role in determining whether cells can metastasize. The research found that curved edges and corners activate cancer stem cells, which are responsible for spreading cancer to other tissues.
Researchers found that breast cancer cells spread by sliding around other cells blocking their escape route out of the original tumor. The study identified molecular pathways that regulate cell-sliding behavior and showed that increased levels of E-cadherin can diminish this behavior.
Researchers found that orchestrated cell death mechanisms in pancreatic cancer can induce the growth of tumor cells by suppressing the immune system. Inhibiting these pathways may reverse immunosuppressive environments and enable T lymphocytes to attack tumors.
A biomarker associated with basal cell carcinoma, EZH2, has been identified in a study published in JAMA Oncology. Higher levels of EZH2 and Ki67 were found in more aggressive tumors, suggesting that the protein may serve as a marker for increased cancer recurrence or tumor aggressiveness.
A new cancer treatment approach uses microparticles and mesenchymal stem cells to deliver chemotherapy directly to tumor cells, reducing systemic toxicity. The method successfully kills tumor cells via a strong bystander effect, offering hope for targeted treatment of prostate cancer and potentially other diseases.
PharmaMar showcases new compounds with unique mechanisms of action against solid and hematological tumors. Lurbinectedin attacks the microenvironment, Plitidepsin targets eEF1A2 protein, and PM184 disrupts blood vessels, cutting off nutrient and oxygen supply to tumor cells.
This special issue on cancer metastasis features groundbreaking research on tumor development, spread, and treatment resistance. Studies reveal the role of hypoxia, neutrophils, and genetic evolution in promoting metastasis, as well as potential therapeutic targets for prevention and treatment.
Researchers at CRI identified a new metabolic pathway that allows cancer cells to survive in conditions toxic to normal cells. The study reveals that cancer cells use an alternate version of the pentose phosphate pathway and the Krebs cycle to defend against reactive oxygen species.
Research shows that aged tumor cells in melanoma are more metastatic and resistant to treatment with targeted therapies due to changes in the microenvironment. Antioxidants, such as N-acetylcysteine, may be a better treatment strategy for older patients.
Researchers found that dozens of targeted therapies inhibit T cell activity, which can help fight tumors. However, pairing these drugs with an IL-15 superagonist stimulates T cell activity, preserving cancer-blocking effects. The study suggests a potential way to overcome immunosuppressive effects while maintaining anti-cancer benefits.
Researchers at Kyoto University's Yamada lab created a mouse model to study the EWS-FLI1 gene's role in bone cancer. The model revealed that other mutations are necessary for cancer development and that correcting osteogenic cell differentiation could prevent bone cancers.
Researchers used optogenetics to manipulate bioelectrical signals in cells, preventing tumor formation and inducing regression. This breakthrough provides proof of principle for a new class of therapies that use light to target tumors, potentially avoiding toxic chemotherapy.
Researchers have found a correlation between hypogonadism and high Gleason scores in prostate cancer patients. This association could help predict patient outcomes before surgery, allowing for more targeted treatment strategies.
Researchers identified a critical connection between the cancer-related gene Myc and cell-surface molecules that protect tumors from the immune system. The study found that reducing Myc expression led to lower levels of protective proteins CD47 and PD-L1 on tumor cells, enabling them to evade immune detection.
A recent study by MIT biologists found that cancer cells use amino acids to build new cell mass, contradicting the long-held assumption that glucose is the primary source. The largest contributors to cell mass were amino acids, making up 20-40% of total mass.
A recent study shows that cancer cells work together with surrounding healthy cells to build new blood vessels, promoting tumor growth. Researchers found that collagen production is increased by a specific type of transfer RNA, allowing tumors to acquire the necessary resources to grow and spread.
Researchers found PGK1 plays a key role in coordinating cellular processes for cancer metabolism and brain tumor formation. The enzyme promotes energy production through the Warburg effect, leading to rapid cancer growth.