Researchers at CNIO successfully applied CRISPR technology to eliminate fusion genes causing tumors, leading to the death of cancer cells while leaving healthy cells unaffected. This breakthrough approach could lead to the development of targeted cancer therapies.
A genome-wide association study has identified genetic markers associated with a higher risk of developing capecitabine-induced hand-foot syndrome. The study found that patients with low levels of R-cadherin and involucrin were more likely to experience severe skin symptoms.
Researchers from CNIO achieved complete remission in 25% of lung tumors induced by KRAS oncogene in mice following genetic inactivation of CDK4 and RAF1. This strategy also prevented cancer cell growth in healthy mice and identified molecular mechanisms that triggered resistance, such as PI3K pathway activation.
Research led by Daniel Lietha has uncovered the structural basis of Focal Adhesion Kinase (FAK) activation on lipid membranes. FAK is activated when localized to the cell membrane, where it interacts with specific phosphoinositide lipids, leading to autophosphorylation and activation.
Researchers identify essential cohesin STAG2 in mouse embryonic development, while its inactivation is detrimental to adult health. The study provides substantial evidence of the specific functions performed by different cohesin subunits.
Researchers at CNIO develop effective therapy for mice with age-related pulmonary fibrosis, activating telomerase production to prevent disease development. The treatment, a gene therapy, also successfully reversed fibrosis in mice without genetic alterations.
A research team from CNIO and HKUST has discovered a specific genetic alteration in some glioma patients that evades the combined therapy, leading to resistance. The study provides clues on how to monitor therapy efficacy and may lead to changes in treatment methods.
International laboratories joined forces to create BrMPanel, a repository of over 60 cell lines for brain metastasis research. The platform facilitates knowledge exchange and speeds up the development of effective therapies.
A new protocol enhances stem cells' ability to differentiate into adult cells, improving their quality and efficiency for therapeutic purposes. The study identified microRNA 203 as a key molecule to boost stem cell differentiation, opening doors to improved treatments for degenerative diseases.
A CNIO-led European study has confirmed that diabetes type 3c is an early manifestation of pancreatic cancer, allowing for earlier diagnosis and treatment. The study found that pancreatic cancer is the cause of the development of diabetes type 3c in 26% of cases.
A recent study by the CNIO reveals that rapamycin can worsen diseases associated with short telomeres, but may be beneficial in other cases. The researchers found that mice with short telomeres are more sensitive to nutrients and hyper-activated mTOR pathway.
Researchers at CNIO propose a novel approach using CDK4/6 inhibitors after chemotherapy to prevent tumor cells from resisting treatments. This strategy shows promising results in preventing tumor growth and death in mice with pancreatic adenocarcinoma, suggesting new avenues for improving cancer treatment.
Researchers from CNIO and Cabimer reveal DNA topological problems cause endogenous DNA breaks leading to lymphoma development. The study highlights a strong causal relationship between topological problems and cancer development in ATM-deficient lymphoid malignancies.
Researchers at CNIO have identified a potential effective treatment for sarcomatoid mesothelioma, the most aggressive type of asbestos cancer, using two existing drugs in combination. The study found that blocking MEK and PI3K pathways reduces the growth and invasiveness of mesothelioma cells in mice.
A team of researchers led by Miguel Quintela-Fandino has discovered the link between FASN and cancer development. They found that FASN is essential for anchorage-independent growth, a hallmark of cancer transformation.
Researchers have successfully created mice with hyper-long telomeres, which live longer and healthier lives without any genetic modification. This breakthrough shows that lengthening telomeres can increase longevity and delay metabolic ageing, paving the way for potential future treatments.
Researchers at CNIO and the University of Würzburg have solved the 3D structure of the T7SS nanomachine used by Mycobacterium tuberculosis to evade the immune system. This finding provides crucial information for developing new therapeutic strategies against tuberculosis, a disease that kills over 1.6 million people worldwide each year.
Researchers from CNIO developed stable long-term cultures of mouse urothelial cells, enabling the study of biological mechanisms underlying bladder cancer. They identified a small population of stem cells that gives rise to cancer, providing new insights into disease development and tissue regeneration.
Follicular lymphoma originates from mutations in RagC gene on mTOR signalling pathway, affecting B cell growth. Rapamycin treatment delays progression and prolongs survival in mice with RagC mutations.
Researchers at CNIO have developed a method to isolate haploid mammalian cells with half the number of chromosomes, enabling efficient genetic research. Chemical compounds like DAB selectively favor haploid cells over diploid ones, promoting cell growth and replacement.
Researchers at CNIO discover cohesin's new functions in pluripotency and genome architecture, shedding light on cancer development and rare diseases. Cohesin-SA2 regulates Polycomb domains, maintaining chromatin organization.
CNIO researchers identified new drug combinations that prevent therapy resistance in mice with glioblastoma by targeting the RAS pathway and telomere maintenance. The study found effective synergistic effects and increased life expectancy in mice by up to 80%.
Researchers from CNIO have found that high levels of URI protein protect mice from radiation-induced intestinal damage, while low or no detectable levels lead to gastrointestinal syndrome and death. The study opens up new avenues for treating and preventing gastrointestinal syndrome by inhibiting c-MYC.
A study published in JNCI has identified hnRNP K as an oncogene that may cause B-cell lymphomas. The overexpression of this tumour suppressor gene was found to promote the development of cancer, leading to poor recovery and low survival rates for patients.
Researchers at CNIO describe the RUVBL1-RUVBL2 ATPases as the 'energy engine' in the co-chaperone R2TP, regulating access to ATP for energy production. The study found a gate-like structure in RUVBL2 that controls energy exchange, coupled to the assembly of mTOR complexes.
Researchers at CNIO have discovered biomarkers in surgically treated patients' fluid that reveal specific mutations and help determine cancer recurrence risk. The new liquid biopsy technique may enable earlier detection and more targeted treatment for melanoma patients.
Researchers from CNIO have successfully removed advanced pancreatic ductal adenocarcinoma (PDA) in animal models through combined inhibition of EGFR and c-RAF kinase. This breakthrough has shown significant promise for developing new cancer treatments.
Researchers from the CNIO Hereditary Endocrine Cancer Group have identified a new gene, DLST, involved in the development of paragangliomas and phaeochromocytomas. Mutations in this gene were found to be directly linked to the disease, providing a potential breakthrough in diagnosis and treatment.
A recent study has found that Focal Adhesion Kinase (FAK) acts as a sensor to mechanical forces generated by the cytoskeleton, activating biochemical signals regulating cell migration. This discovery provides new insights into how cancer cells invade and metastasize, potentially leading to therapies targeting this mechanism.
Researchers identified a link between BRCA2 mutations and aggressive prostate cancer in men, increasing their risk of developing other cancers. The study also found that patients with BRCA2 mutations have poorer treatment responses and outcomes.
A comprehensive study reveals that p62 protein controls multiple factors involved in melanoma metastasis, indicating a coordinated process. The research also identifies FERMT2 as a marker for poor patient prognosis.
Researchers at CNIO and Hospital 12 de Octubre have discovered a potential new combination therapy for myelofibrosis, a severe haematological disease. The three-drug combination of nilotinib, prednisone, and ruxolitinib enhances the treatment's effectiveness by potentiating each other's benefits.
A clinical trial led by CNIO's Luis Paz-Ares showed that immunotherapy significantly increases patient survival when administered alongside conventional chemotherapy. This opens the door to investigate its effectiveness in early stages of the disease.
A study led by CNIO has defined a blood-based biomarker that can determine the most effective treatment for castration-resistant prostate cancer patients. The biomarker, which analyzes the presence of a specific gene in circulating tumour DNA, shows promise for improved survival rates and personalized therapy.
Researchers will identify biomarkers for DNA repair defects in tumors, enabling faster decision-making on treatment choices. A clinical trial will test carboplatin therapy's effectiveness in advanced prostate cancer.
Researchers at CNIO have linked the protein MASTL to a type of inherited thrombocytopenia, which may lead to breakthroughs in cancer metastasis research. They discovered that manipulating other enzymes could potentially reverse the defect and explored its therapeutic potential.
A new international collaboration led by the CNIO reveals that up to 20% of human genes may not be coding genes, but rather non-coding or pseudogenes, which could have significant effects on biomedicine. The study analyzed gene catalogs and found that many genes were more likely to be non-coding than previously thought.
Researchers identified six protein kinases that predict the evolution of triple negative breast cancer, allowing for new pharmacological targets and potential treatment combinations. The study's findings indicate a high cure rate (95%) for patients with no activated proteins, but increased relapse risk if one or more are active.
Researchers at CNIO develop gene therapy with telomerase, proving effective in mice against diseases caused by excessive telomere shortening. The study finds that the gene therapy does not increase the risk of developing cancer, even in a cancer-prone setting.
Researchers have discovered that PLK1 acts as a tumor suppressor in some breast tumors, halting development and changing prognosis. This finding was made by researchers from CNIO and DKFZ.
A study led by CNIO researchers shows that silibinin reduces brain metastasis lesions in mice and patients, targeting the tumor microenvironment. The treatment has shown encouraging results, with 75% of patients reacting positively and a 15.5-month average survival rate
Scientists discovered that altered cohesin SA2 variant influences gene expression and favours loss of differentiation in tumour cells. The two cohesin variants have distinct functions, with SA1 involved in topological domains and SA2 regulating gene expression through local chromatin loops.
A novel data-driven approach called PanDrugs prioritizes cancer treatments based on patient genetic alterations. The method integrates pathway context and collective gene impact to provide therapeutic options for patients with limited druggable genes.
Research by Maria A. Blasco and colleagues reveals TERRAs interact with the Polycomb complex to assemble telomeric heterochromatin. In cells deficient for TERRA, telomeres show decreased heterochromatic marks, indicating a crucial role in telomere protection and maintenance.
A study published in the Genes & Development journal reveals that tumor cells can survive even without Ras genes if Erf is also lost, casting doubt on the effectiveness of potential treatments. The researchers found that eliminating ERF allows mouse stem cells to grow and differentiate in the absence of RAS genes.
Researchers have determined the high-resolution structure of R2TP, a complex involved in key processes for cell survival. The study reveals that R2TP forms complexes with mTOR and other related kinases by interacting with HSP90.
Researchers developed a powerful mouse model using CRISPR-Cas9 and RCAS/TVA system to mimic glioma genetic alterations. The model enables the study of gene fusions and mutations in cancer progression and treatment response.
Researchers at CNIO discovered that a gene controlling inflammation also increases pancreatic cancer risk. The study suggests new strategies for prevention and detection of the disease.
CNIO researchers have identified a subpopulation of cancer-associated fibroblasts that foster tumour growth and discovered the Saa3 gene as a key player. Eliminating this gene reprograms the cells, losing their pro-tumour properties, opening a new avenue for therapeutic strategies.
Researchers develop a genetic model that eliminates c-Raf kinase, causing tumor regression with low toxicity; validation opens new possibilities for therapies against KRAS-driven cancers. Lung cancer remains a leading cause of cancer-related deaths worldwide.