Research on the biology of tumor cells. Covers tumor spread, cell-particle diagnostics, new anti-tumor molecules, and cancer-killing immune cells.
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.
A study published in Science reveals a key role for the protein H1.0 in turning cancer tumor cells into cancer stem cells with the ability to sustain long-term growth and cause recurring disease outbreaks. The discovery could lead to medical interventions targeting these cells to prevent cancer spread.
Researchers have developed a method to measure the mechanical force that cancer cells exert on their fibrous surroundings. This study found that as cancerous cells migrate through 'cross-talk' with the matrix, it stiffens, causing the cell to pull harder and potentially promote metastasis.
Researchers found that triple-negative breast cancer cells are addicted to cystine and die rapidly when deprived of it, suggesting a potential new treatment. Cystine-blocking molecules may be effective in targeting this pathway, which is also used by other aggressive cancers.
A study published in Nature Genetics found that certain genetic mutations more frequently occur in male cells, potentially leading to cancer. The researchers identified six genes on the X chromosome that are more likely to be mutated in males, suggesting a new theory behind the sex disparity in cancer incidence.
Research reveals that childhood brain tumors originating from undifferentiated stem cells are more frequent and aggressive than those from oligodendrocyte precursor cells. Tumor cells from stem cells also show increased susceptibility to cancer drugs, according to a new study published in Cancer Research.
Researchers have discovered that the NAALADL2 molecule, which indicates more aggressive prostate cancer, can also be used to guide treatments. This new marker has the potential to distinguish between slow-growing and fast-growing prostate cancers.
Researchers silenced SIRT2 to accelerate the degradation of Slug protein, reducing tumor growth and invasiveness in basal-like breast cancer cells. The study revealed a direct relationship between SIRT2, Slug stability, and malignant behavior, providing new insights into treating aggressive basal-like breast cancers.
Researchers link PIP to cell-mediated immunity, suggesting its potential as a new target for immunotherapeutic agents. PIP may help the immune system recognize and destroy foreign cells, including tumor cells, offering a protective effect against breast cancer.
Researchers at Uppsala University developed a new approach to study cancer cells' reactions to treatments, enabling the identification of promising drug combinations. 3D tumor models mimic real-world conditions, where cancer cells have limited access to nutrients and oxygen.
A small molecule can turn short-lived T-cells into long-lived, renewable cells that destroy tumour cells. Researchers have identified a way to increase the life-span of these T-cells, overcoming a key hurdle in immunotherapy.
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
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.
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.
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 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 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 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.
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.
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 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.