Articles tagged with Tumor Cells
Researchers at University of California San Diego School of Medicine found that cancer cells exploit the unfolded protein response (UPR) to activate Wnt signaling, promoting tumor survival and drug resistance. This mechanism enables cancer cells to cope with nutrient deprivation and therapies, contributing to intra-tumor heterogeneity.
Researchers at German Cancer Research Center (DKFZ) found a substance that blocks cancer-promoting metabolic products in leukemia and brain tumors. The investigational compound BAY1436032 is effective against AML and glioblastomas, reducing stem-cell properties and tumor cell growth.
Researchers have developed a chemical array technique that can identify and culture malignant stem-like cells within melanoma tumors. This allows for the creation of patient-specific models for individualized cancer treatment.
Moffitt researchers demonstrate that mathematical models can be used to predict how different tumor cell populations interact with each other and respond to environmental changes. By applying small biological forces, they show that complex systems like cancer can be steered into a less invasive growth pattern.
AbeXXa Biologics identifies targets for cancer treatment from thousands of intracellular proteins, potentially resulting in effective immunotherapies for broad patient groups. The company is developing T cell receptor-like antibody-drug complexes to kill tumor cells with low peptide/HLA targets.
Researchers used C. elegans to identify a genetic signature of mesodermal-epithelial communication involved in human cancer cell proliferation. The study uncovered 33 genes conserved between worms and humans that control this network, providing a roadmap for new cancer therapies.
A study published on Nature Communications reveals that breast cancer cells undergo a stiffening state prior to acquiring malignant features and becoming invasive. This discovery identifies a new signal in tumor cells that can be further explored when designing cancer-targeting therapies.
Researchers discovered that residual tumor cells display alterations in fat metabolism and oxidative stress, which contribute to DNA damage and cancer relapse. Targeting metabolic pathways in these cells could potentially prevent recurrence.
Researchers at EMBL found that residual breast cancer cells have specific traits that distinguish them from healthy cells and seem to cause relapse. The study suggests lipid metabolism as an exciting therapeutic target to reduce breast cancer recurrence.
Research reveals how hypoxia leads to inhibition of miR-34a, a key tumor suppressor, promoting metastasis and EMT. The findings suggest that targeting this process with drugs could be a therapeutic approach for treating metastasizing colon tumors.
Researchers discovered that blocking this Wnt pathway prevents tumor growth and prolongs mouse lifespan. Human lung adenocarcinoma samples also showed high levels of Wnt activation.
Scientists have pinpointed two molecules, FOXG1 and SOX2, that drive glioblastoma cells' rapid division and prevent specialization. These findings could lead to the development of new therapies targeting these molecules to slow or stop tumour growth.
In liver cancer, Scrib's increased expression suppresses the growth of cancer cells by inhibiting three oncogenes. The study provides the first hard evidence that Scrib functions as a tumor suppressor in human and animal liver cancer.
Scientists develop a hybrid nanomaterial that releases a free-radical-generating prodrug inside tumor cells, destroying them even in oxygen-depleted conditions. The material damages cells by a ROS-type radical mechanism without the need for oxygen.
Researchers discovered that tumor cells in patients with advanced prostate cancer are reprogrammed, reducing response to anti-androgen therapy and creating more aggressive tumors. SOX11 acts as a key regulator in this process, which may be targeted for new treatments.
Scientists at Scripps Research Institute discovered that invasive tumors can send out tumor cells earlier than thought, which may seed secondary tumors years later. The escaping cells enter the bloodstream by entering blood vessels deep within the dense tumor core, upending the long-held belief about metastatic cell origin.
Joslin Diabetes Center researchers found impaired insulin effects boost cancer risks in mice with genetically modified intestinal tumors and blood vessels. Insulin resistance may impair blood vessel health and share biological mechanisms with cardiovascular disease.
Researchers Melissa Skala and Matthew Vander Heiden won a $250,000 award to study the interaction between tumor cells and healthy supporting cells in pancreatic cancer. The project aims to create molecular changes that shut down the tumor's ability to scavenge nutrients, potentially leading to a new type of metabolic cancer therapy.
Scientists discover that physical arrangement of cells drives cell death and removal, with topological defects causing cells to realign and leading to extrusion. This finding provides new insights into tissue development and control of cell growth.
Wake Forest Baptist researchers found that MIR506 inhibits malignant cell growth and metastasis in pancreatic cancer cells. The molecule induces autophagy, a process that promotes cancer cell death.
A study at Massachusetts General Hospital found that two major types of brain tumors, astrocytomas and oligodendrogliomas, may originate from the same type of neural progenitor cells. The analysis revealed differences in gene mutation patterns and tumor microenvironments between the two subtypes.
Researchers at Tokyo Medical and Dental University developed a new process to improve the detection of cancer stem cells in brain tumors. The approach uses iron chelation to increase fluorescence levels, allowing for more accurate identification and removal of these cells. This breakthrough has potential to translate to clinical practice.
A study led by Raffaella Sordella proposes a novel theory on how cancers circumvent targeted therapy killing power. The research suggests that genetic diversity in tumor cells, caused by non-genetic mechanisms, can help them survive and eventually relapse.
A study published in Briefings in Functional Genomics investigates the role of epigenetics in cancer development, showing that disruptions can activate oncogenes or shut down tumor suppressors. The paper also highlights the link between epigenetic changes and metabolites, which can target and amplify gene expression.
Researchers defined cell-type composition of cancerous cells from 11 colorectal tumors using single-cell genomics and computational techniques. The study identified two distinct subtypes of cancer-associated fibroblasts that contribute to a worse prognosis in colorectal cancer patients.
Researchers at MIT developed a strategy to make tumor cells more susceptible to certain types of cancer treatment by coating them with nanoparticles. The particles increase the forces exerted on the cells, making them more likely to die, and were found to be 50% more effective in tests in mice.
Scientists at IDIBAPS and IRB Barcelona developed a novel strategy to genetically modify viruses that selectively target tumor cells while sparing healthy tissue. The study's results show promising effectiveness in controlling tumor growth and destroying cancer cells, offering hope for new cancer therapies.
A new computational method allows researchers to quickly compute immune cell infiltration and calculate personal immune response profiles for thousands of patients. The study reveals complex interactions between different immune cell types in the tumor microenvironment play meaningful roles in patient survival.
Researchers at Medical University of South Carolina found that inhibiting moesin reduces numbers of regulatory T cells, enabling the immune system to see and attack cancer. This could lead to new treatments for cancer and Treg-related immune disorders.
Researchers found high levels of activated Notch in tumor endothelium, promoting cancer cell invasion into bloodstream and forming lung metastases. Blocking Notch with antibodies reduced metastasis and immune cell invasion.
Researchers discovered that weakly adherent cancer cells are more likely to migrate and invade other tissues compared to strongly adherent cells. This finding suggests that adhesion strength may serve as a general marker of metastatic cells.
Researchers identified PAK1 as a key player in aggressive tumor growth, fibrosis, and chemotherapy resistance. Targeting PAK1 may increase survival rates for patients with pancreatic cancer.
Researchers found that cancer cells can spread through the extracellular matrix with optimal tissue stiffness. Drugs targeting ECM stiffness could prevent metastasis, providing a new approach to diagnostics and treatment.
Prostate cancer cells grow with malfunction of cholesterol control in cells, a process that allows them to accumulate fat and stimulate uncontrolled growth. Identifying this process could inform the development of better ways to control cholesterol accumulation in tumors.
Scientists at Trinity College Dublin discovered how cancers hijack the immune system's wound-healing response to receive help. They found that a molecule called TRAIL can be re-wired in certain tumors to send an inflammatory signal, tricking the immune system into assisting cancer growth.
Researchers at IDIBELL have developed an oncolytic virus that redirects the patient's immune system against tumor cells, increasing antitumor efficacy. The virus uses BiTE antibodies to activate T lymphocytes and capture them to attack adjacent cancer cells.
Researchers identified a gatekeeper protein SMARCB1 that prevents aggressive pancreatic cancer cells from transitioning into a resistant type. Depletion of SMARCB1 leads to mesenchymal status, a mobile and invasive cell state, making these cells vulnerable to therapies targeting proteostasis.
A University of Colorado Cancer Center study characterizes the uptick of myeloid-derived suppressor cells in human cancer patients' spleens, revealing their immunosuppressive function. Higher splenocyte counts were associated with increased risk of death and decreased overall survival.
Researchers at OHSU developed a method for quickly mapping single cell genomes, expanding the analysis of cancerous tumors and other diseases. This breakthrough enables precise targeting of cancer cells, offering new avenues for personalized medicine.
A new technique called MATQ-seq increases the accuracy of detecting gene expression in single cells to 90%, allowing scientists to study how cancerous tumors begin and potentially uncover better treatments, diagnosis, and prevention strategies.
Researchers at Uppsala University discovered a correlation between brain tumor cell origin and its growth rate, malignancy, and response to cancer drugs. The study found that tumors originating from immature neural stem cells were more aggressive and less sensitive to treatment than those from differentiated glial cells.
Researchers at Massachusetts General Hospital have found that tumor necrosis factor receptor type II (TNFR2) may be a major target for immuno-oncology treatments. The team's findings suggest that blocking TNFR2 could restore the ability of a patient's immune system to attack tumors, while also directly killing cancer cells.
Researchers at Trinity College Dublin have discovered a link between the loss of miR-17 and oesophageal tumour resistance to radiotherapy. Higher numbers of cancer stem cells formed larger, more aggressive tumours and were more resistant to radiation-induced cell death. Synthetic miR-17 may enhance radiotherapy effectiveness in patients.
Researchers found that cells with an extra chromosome grew more slowly and formed smaller tumors than comparable cells with normal chromosome number. However, after weeks of growth, these cells rapidly evolved to acquire new mutations that enabled them to grow rapidly.
A research team at Nanjing University found that PKM2 promotes exosome release by phosphorylating SNAP-23, which controls the dock and release of secretory granules or exosome-containing multivesicular bodies. This study demonstrates for the first time that PKM2 plays an essential role in promoting tumor cell exocytosis.
Researchers have discovered how cancer cells convert into blood vessel-supporting cells that drive tumor growth. The process of epithelial-to-mesenchymal transition (EMT) sustains blood vessels and fuels tumor expansion.
Researchers at Penn have identified a mechanism by which mitochondria can drive changes in nuclear gene expression associated with tumor progression. The epigenetic process involves a protein triggered by mitochondrial oxidative or metabolic stress, leading to reduced cancer gene expression when blocked.
Researchers from Ruhr-University Bochum found that capsaicin, an active ingredient in chilli peppers, inhibits the growth of triple-negative breast cancer cells by activating the TRPV1 receptor. The treatment also causes tumour cells to die and reduces their ability to form metastases.
Researchers found that fibrosarcoma cells can't perform piston movement to get through tight squeezes, leaving them intact while normal cells use molecular motors to muscle forward.
Scientists at The Wistar Institute have identified a novel protein pathway in mitochondria that controls energy production for cell invasion and metastasis across multiple cancer types. This pathway, previously observed in neurons, has strong clinical implications and represents a potential therapeutic target for several types of cancer.
Researchers found that KRAS mutant cancer cells form more stress granules in response to chemotherapy, making them harder to kill. A new compound target, 15-d-PGJ2, may help improve treatment outcomes by blocking this coping mechanism.
A new method has been developed to identify suitable protein structures directly from patients' tumor cells using mass spectrometry. This approach allows for the identification of mutated peptides presented on the surface of cancer cells with high accuracy and speed.
Researchers have developed biocompatible nanocapsules that transport glucose oxidase and L-arginine into tumor cells, starving them of nutrients while releasing toxic nitrogen monoxide. This synergistic treatment concept successfully inhibits cell growth, initiates cell death, and shrinks tumors in mice.
A new blood test may provide a cheap and effective way for doctors to manage lung cancer by analyzing genetic profiles of tumor cells in patient blood samples. The test is safer, cheaper, faster, and more effective than alternative diagnostic approaches, costing less than $30.
A team of scientists tracked the genetics of disseminated tumour cells in breast cancer patients, finding they are genetically similar to the original tumour. This knowledge could help clinicians choose the most effective therapy, potentially leading to better outcomes and a more accurate prognosis.
Three researchers were awarded the Brupbacher Cancer Research Prize for their work on epigenetics, which regulates gene activity and is linked to cancer development. The team's findings suggest that epigenetic changes can trigger abnormal gene inactivation in tumor cells.
Researchers at IRB Barcelona identify CD36 as a general marker of metastatic cells, which are responsible for initiating and promoting metastasis in several types of human tumors. High-fat diets have been shown to enhance the formation of metastases in mice inoculated with oral cancer cells.
Researchers identified altered genes and noncoding genetic material that could serve as predictive treatment biomarkers or targets for therapy. The study found that ATRX mutations were associated with aggressive NF1-related brain cancers, while a microRNA called miR-487b was underexpressed in tumor tissue.
ADC MI130110 shows remarkable antitumoral activity in CD13-expressing tumor cells, impairing tubulin polymerization and disrupting the microtubule network. The treatment resulted in significant reduction in tumor size, complete remission, and increased median survival time.
The grant will help TGen accelerate the computer processing of transcriptomes from thousands of cells using a complex computational algorithm. This process will advance precision medicine by quickly informing doctors with the best options for attacking each individual patient's cancer.