A high-protein diet can protect against colorectal cancer in those with inflammatory bowel disease, while a low-protein diet may be beneficial for those with a genetic predisposition. Researchers suggest tailoring treatments based on the amount of protein in the diet.
Scientists have discovered a novel mechanism that prevents glioblastoma development through the modulation of EFGR expression by RanBP6. The study reveals that silencing of RanBP6 promotes glioma growth by upregulating EGFR expression, while reconstitution of RanBP6 leads to reduction in tumor growth.
Researchers have developed a new therapy that blocks the TRF1 protein, which is essential for protecting telomeres in glioblastoma cells. This approach has shown promising results in mouse models, with a significant increase in survival rates and reduction in tumour growth.
Researchers have identified a connection between the PI3K pathway and telomere protection, revealing a potential target for cancer treatment. Inhibition of PI3K reduces TRF1 levels, leading to chromosome destabilization and cancer cell death.
Researchers discover genetic alteration directly involved in at least 10% of T-cell acute lymphoblastic leukemia cases. The Capicua gene acts as a tumour suppressor and is linked to resistance to certain treatments.
Researchers at CNIO have developed a way to stabilize haploidy in animal cells, overcoming the issue of quick loss of genetic stability. By removing the p53 tumor suppressor gene, the group increases the survival rate of these cells, thereby stabilizing their haploid state.
Researchers found that a kinase-inactive Braf mutant triggers lung adenocarcinoma in mice, and co-expression of oncogenic Kras enhances tumor initiation. Additionally, individual Braf inactivating mutations are also oncogenic events. These findings suggest a potential therapeutic strategy for lung cancer patients with hypoactive BRAF.
Researchers have discovered new genes associated with the development of pheochromocytomas and paragangliomas, which are rare neuroendocrine tumors with a strong hereditary component. The study identifies alterations in enzymes involved in cell respiration as a key factor in tumor growth.
Elena Castro, a Spanish researcher, is awarded the Prostate Cancer Foundation's Young Investigator Award for her project on DNA damage repair genes and their impact on advanced prostate cancer progression. The award supports her work to develop therapeutic strategies for patients with genetic defects.
Researchers at CNIO found that Plk1 inhibitors can cause hypertension and severe cardiovascular problems, suggesting a need for more thorough studies on protein functions. The study used laboratory mice to model human diseases, revealing the critical role of Plk1 in maintaining blood pressure.
Research reveals a link between Alzheimer's and lower lung cancer risk due to mitochondrial dysfunction and chronic inflammation. A study analyzing over 1000 patient samples identified altered genes and confirmed the protective effect of Alzheimer's against lung cancer.
Researchers at CNIO have developed a technique to study melanoma progression in mice, revealing unknown mechanisms and identifying new markers of metastasis. The MIDKINE protein has been identified as a key factor in melanoma metastasis, representing a new therapeutic target.
The article reviews current chemical search engines, named entity recognition and text mining systems to efficiently access biomedical data. Researchers emphasize the need for structured databases to process unstructured data in scientific literature, clinical reports, and patents.
The LimTox tool provides information on drug hepatotoxicity extracted from biomedical archives, enabling efficient associations to adverse reactions. It offers keyword searches and entity-specific queries for researchers and clinicians, promoting targeted search queries and biological knowledgebase construction.
A CNIO researcher has been funded by the Melanoma Research Alliance to study brain metastasis in melanoma, focusing on blocking cancer cell spread by targeting the microenvironment. The goal is to develop a new concept of treating metastasis in personalized medicine.
Researchers create a cellular model of Ewing sarcoma in human stem cells using CRISPR technology, enabling the study of mechanisms underlying the disease. The technique improves upon previous methods, increasing success rates by up to seven-fold and opening new avenues for cancer research and potential treatment.
Researchers have discovered that excessive DNA replication can lead to cell malignancy but also offers a potential approach against cancer. By exploiting the cooperation of proteins CDC6 and CDT1, scientists aim to induce lethal DNA re-replication selectively in cancer cells.
Research reveals liver progenitor cells become activated and expand due to oncogenic signals from malignant hepatocytes. Progenitor cells can lead to benign or aggressive tumours, contributing to tumour heterogeneity.
A new study links protein c-Fos to liver carcinogenesis, highlighting the importance of maintaining healthy cholesterol levels in preventing liver cancer. The research suggests that statins may also prevent deleterious changes in hepatocytes caused by hypercholesterolemia and reduce inflammation.
Researchers have identified pre-metastatic niches that prepare the ground for tumor cells to survive before invading other organs. Understanding this phenomenon could lead to new diagnostic and therapeutic tools to prevent cancer-related death.
In vivo reprogramming induces signs of telomere rejuvenation, reversing aging's hallmark: short telomeres. The process involves telomerase activation and elongation, similar to early stages of tumor development.
A study has deciphered many interactions between human proteins using bacterial counterparts, potentially involved in diseases like cancer. The results help clarify molecular details of these interactions.
Researchers at CNIO found that tissue damage enables cells to adopt embryonic features through the OSKM gene system, mediated by proinflammatory molecule IL-6. This discovery could improve regenerative medicine and treatment of degenerative diseases.
Researchers at CNIO have discovered CPEB4, a protein essential for melanoma cell survival and proliferation. The protein regulates the expression of factors unique to this tumour type, making melanomas more vulnerable to drugs targeting this pathway.
The Structural Biology and Biocomputing Programme at CNIO has contributed to the BLUEPRINT project, a major European initiative studying the human epigenome. The project has generated a large volume of epigenomic data, which is now accessible for research, facilitating new ways to diagnose and treat diseases.
Scientists at CNIO deconstructed alternative splicing as a source of protein production, finding it secondary to gene dominance. The study reveals that most human genes produce a single dominant protein, calling for rethinking biological innovation.
The discovery of POLD3's critical role in DNA replication reveals its necessity for both tumor and healthy cells, casting doubt on its use as a therapeutic target for cancer treatment. The study used genetic engineering to eliminate the gene in mice, showing its essential function in cell division and survival.
Researchers have identified the ATG5 protein as a key regulator of metastatic capacity in melanomas. The study found that patients with partial loss of the ATG5 gene have a worse prognosis, developing metastasis and resistance to drugs.
Researchers have identified the precise point of origin for TERRA RNAs, which protect telomeres and maintain chromosomal stability. The discovery sheds light on the importance of TERRA in cell viability and telomere preservation.
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.
Researchers used assortativity to analyze DNA interactions and identify proteins mediating chromatin contact networks. This approach helps understand genome organization and its relationship with gene expression regulation.
CNIO researchers reveal that proinflammatory cytokine IL-17A triggers non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC), two conditions with no current treatment. Blocking IL-17A or inhibiting cells that secrete it may prevent NASH in high-risk patients.
Researchers have identified various miRNAs that can predict the response of metastatic renal cancer patients to anti-angiogenic agents. These biomarkers have been shown to be stable and detectable, allowing for personalized treatment. The study provides a promising tool for improving patient outcomes.
A new study reverses resistance to antiangiogenic drugs by adding an antidiabetic agent, inhibiting tumor growth up to 92%. Researchers found that this mechanism can be targeted to attack cancer cells, with potential for improved treatment outcomes. The discovery has the potential to prolong patient benefit from antiangiogenic treatments.
Researchers at CNIO have developed a new method to create mice with hyper-long telomeres using epigenetic changes, avoiding genetic manipulation. This technique results in fewer signs of molecular aging and a lower incidence of cancer in the mice.
Researchers at CNIO have identified a protein, CDC25A, as a determinant of chemotherapy resistance in cancer cells. They used CRISPR genome editing technology to test various mutations and found that cells with this mutation were resistant to treatment.
Researchers from CNIO have discovered a link between psoriasis and bone loss, finding that the disease causes widespread and progressive bone tissue loss. Treating psoriasis patients with IL-17 blockers could have benefits for bone health, and the study suggests potential implications for other autoimmune disorders.
Researchers found that increasing NADPH levels in cells improved natural antioxidant defenses, reducing oxidative damage and age-related processes. Long-lived transgenic animals showed lower levels of oxidative damage and delayed aging, with increased longevity and better movement coordination.
Researchers at CNIO have discovered a code of signals that regulates the concentration of proteins involved in genome duplication. The USP7 protein acts as a traffic officer, eliminating ubiquitin marks to favor protein accumulation and DNA copying. This balance is essential for accurate genome replication.
Researchers at CNIO have developed a gene therapy to repair telomeres, delaying ageing and potentially treating aplastic anaemia. The treatment uses virus-delivered telomerase enzyme to extend telomeres, increasing blood cell production.
Researchers at CNIO find potential therapy for aggressive type of lung cancer in preclinical models, combining dasatinib and demcizumab to reduce tumour size and improve survival rates. The study uses genetically modified mice and validates effectiveness with human samples, paving the way for clinical trials.
Researchers at CNIO have identified two biomarkers, p21 and mTOR activation, that predict a less aggressive head and neck cancer progression. The study's findings could lead to personalized treatment options for patients.
The study reveals that 5hmC mark acts as a key signal connecting complexes that regulate gene expression, influencing cellular differentiation and energy metabolism in embryonic stem cells. The findings suggest that 5hmC may play a central role in the coordinated evolution of chromatin-related proteins.
Researchers at CNIO have identified a protein called BPTF that is essential for MYC to cause cancer in mouse models, suggesting it could be a new target for future anti-cancer drugs. Inhibiting BPTF reduces the aggressiveness of tumours.
Researchers have identified specific combinations of integrins associated with metastasis to certain organs, including lungs and liver. These 'zip code' proteins guide tumour cells to specific locations, supporting Paget's 'seed and soil' theory.
Researchers have developed a computational method to predict protein dynamics based on co-evolutionary studies, which explains changes in shape or structure to interact with other compounds. This study is crucial for designing drugs and researching genetic diseases like cancer, resulting in higher complexity than current methods.
Researchers have discovered a link between Diamond-Blackfan anaemia and increased cancer susceptibility, using a new animal model that recapitulates key characteristics of the disease. The study found that patients with DBA are predisposed to lymphomas and solid tumours due to mutations in the RPL11 protein.
A study by Juan Méndez at CNIO sheds light on molecular mechanisms of ageing in blood stem cells, opening a new avenue for reducing their decline with age and potentially treating aplastic anaemia. Researchers managed to prevent embryonic lethality by increasing the levels of gene CHK1, showing less pronounced anaemia in mice.
Researchers at CNIO have identified the role of SMC5/6 protein complex in cancer suppression and premature aging, revealing its importance in limiting carcinogenesis and promoting healthy lifespan. The study found that mutations in this complex can lead to tumours and accelerated aging in mice.
Researchers identified a mutated POT1 gene in families with multiple tumors, including cardiac angiosarcoma. The finding opens up the possibility of early diagnosis and treatment for family members.