Researchers have discovered the human enzyme PrimPol, which recognises and repairs DNA lesions during replication, preventing breaks in chromosomes. This ancient enzyme has been found in archaebacteria and is thought to have played a key role in genome evolution and cancer development.
A CNIO study has discovered that genome replication mirrors the evolutionary history of living beings, with older genes replicating first. This model suggests that new genes emerge in later stages of genome replication, potentially leading to the development of complex structures and organs.
A study led by CNIO confirms the therapeutic potential of inhibiting Aurora-A in cancer treatment, revealing an increase in dead and senescent cells and premature aging. The research proposes studying cell nucleus volume as a tool for evaluating anti-cancer drug efficiency.
A CNIO team has discovered that senescence, which makes cells stop dividing, also takes place during embryo development to eliminate unnecessary cells. This process, known as programmed senescence, helps shape the body's tissues and organs.
Researchers found that the immune system's JunB gene causes liver cells to become inflamed during hepatitis, leading to irreversible damage. The study proposes a new mechanism by which AP-1 acts as a double-edged sword in the liver, contributing to both viral defense and disease progression.
Acute dendritic cell leukaemia has a poor prognosis due to its rarity and difficulty in treatment. Researchers sequenced the exome of three patients and found mutations in epigenetic genes, which could lead to new therapeutic approaches.
Researchers discovered two variants of Pds5 proteins that modulate cohesins' behavior, essential for proper cell division. Understanding this regulation can improve diagnosis and treatment for cancer patients and Cornelia de Lange Syndrome sufferers.
Researchers at CNIO have sequenced the exome of 17 patients with non-infiltrating bladder cancer, revealing new genetic pathways and genes involved in the disease. These findings provide a first step towards understanding the biology of bladder cancer and improving patient management.
Researchers at CNIO discovered that Fra-1 protein protects the liver from drug-induced damage and neutralizes toxins. This new regulatory mechanism could lead to future studies on new drugs for diseases related to toxic compound accumulation.
Researchers at CNIO's Cell Division & Cancer Group have discovered that the protein Greatwall is essential for preventing mitotic collapse in mammals. By inhibiting Greatwall, cells can no longer divide properly, which may lead to slowed-down cancer growth and potentially reactivated tumour suppressor PP2A
Researchers discover that increasing c-Fos expression in the skin promotes the development of squamous cell carcinomas, a highly aggressive type of skin cancer. Anti-inflammatory drugs can decrease tumor progression by blocking the immune response induced by c-Fos.
Researchers from CNIO successfully produce embryonic stem cells directly from living adult mice, exhibiting primitive totipotent characteristics and broader differentiation capacity than in vitro-derived cells.
Researchers discovered that over 70% of bladder tumours display somatic mutations in the TERT gene, a protector of genetic material involved in cellular ageing and cancer. The study suggests that these mutations may occur early in the carcinogenesis process, with potential implications for diagnosis and treatment.
Researchers at the Spanish National Cancer Research Centre (CNIO) have discovered a link between telomere protection and obesity, with the RAP1 gene playing a key role. The study found that mice lacking RAP1 gained weight and developed metabolic syndrome, highlighting a new potential mechanism in human obesity.
CNIO researchers describe molecular bases of resistance to PARP inhibitor drugs in familial breast and ovarian cancers. Secondary mutations in genes like 53BP1 or PTIP can compensate for BRCA1/2 mutations, rendering drugs ineffective.
Researchers from CNIO describe how a genetic duplication 500 million years ago led to the evolution of the ASF1b gene, essential for proper cell division and related to breast cancer. The study's findings highlight the importance of studying molecular history to understand gene adaptation in cancer.
Researchers from Spain and the US have identified nine molecular hallmarks of aging, including genomic instability, telomere shortening, and epigenetic alterations. By understanding these hallmarks, they hope to develop treatments that can combat cancer and other diseases linked to aging.
CNIO researchers discovered a new gene called TRF1 that plays a vital role in nuclear reprogramming. This discovery is crucial for understanding the mechanisms of cell differentiation and regeneration, and may lead to breakthroughs in regenerative medicine.
CNIO researchers have successfully mapped the proteins involved in human DNA replication, a process targeted by many chemotherapeutic agents. The study provides new insights into the mechanisms underlying cancer cell division and holds promise for developing new therapeutic strategies.
Researchers identified BRCA2 gene mutation as first genetic factor for prostate cancer prognosis, associated with advanced disease and higher mortality rates. The study suggests a need for new treatment strategies for patients carrying these mutations.
An international study has identified up to 80 new regions of the genome associated with increased susceptibility to breast, prostate, and ovarian cancers. Researchers have also discovered a total of 41 new genes or regions that may contribute to the development of breast cancer.
Researchers have discovered a new mechanism contributing to tumour development, including Chronic Lymphocytic Leukaemia, by identifying mutations in the POT1 gene that affect chromosome protection. This is the first time an essential gene has appeared mutated in human cancer.
Researchers at CNIO have developed new computational methods to study the evolution of proteins and their interactions. These methods enable predictions of molecular relationships and structural changes, with potential applications in cancer treatment and drug development.
Researchers discover collisions between DNA duplication and transcription machineries cause chromosomal alterations in tumor cells. Genomic fragile sites are identified as contributing to genome instability throughout evolution.
A study by CNIO researchers discovered that caloric restriction increases telomere length in adult mice, leading to a lower incidence of cancer and age-related illnesses. The study also found that mice on reduced diets lived up to 20% longer than those with normal diets.
The new age of proteomics brings a comprehensive understanding of cellular proteins, shedding light on their role in illnesses. The next-generation proteomics technology enables improved biomarker search, personalized therapies, and enhanced cancer diagnosis.
Researchers have created two new databases, APPRIS and ChiTaRS, to study the human genome and its variants. The databases contain thousands of genomic variants associated with specific diseases, providing a powerful tool for analyzing mutations in protein variants related to illness.
A team of researchers has discovered that the cellular reprogramming gene SOX2 is directly regulated by the tumor suppressor CDKN1B(p27) gene, which is also associated with cancers such as lung and pituitary cancer. The study also highlights the potential role of adult stem cells in cancer.
Researchers have identified 48 metabolites linked to cellular ageing and disease risk in mice. The study reveals a strong connection between metabolism and biological age, offering new insights into preventive molecular medicine.
A large study published in the Journal of National Cancer Institute has identified a genetic route by which vitamin D may prevent bladder cancer. High levels of 25(OH)D3 in plasma were found to be associated with lower risk of bladder cancer, particularly in patients with more aggressive cancers.
Researchers create precision blood test that uses gene patterns in blood cells to identify advanced-stage prostate cancer patients with worst prognosis. The test can be used to select those in need of immediate treatment.
Researchers have deciphered how a stress-inducible gene regulator, AP-1, controls the survival of liver tumor-initiating cells. Altering these proteins in mice impaired liver cancer development, providing new insights into liver cancer initiation.
A study by CNIO researchers finds that the rate of telomere shortening determines longevity in mammals. Individuals with slower telomere shortening tend to live longer, suggesting a new approach to predicting life expectancy.
Scientists from CNIO describe natural selection at the cellular level, where tissues and organs select the 'best' cells to fend off disease processes. The study reveals the role of haemocytes in eliminating cell residues, shedding light on mechanisms of homeostasis and potential cancer detection.
The CNIO group is part of the Gencode project, creating a reference geneset from Encode data. This effort has mapped four million 'switches' controlling human cell and tissue gene activity, revealing a complex web of interactions.
A CNIO team has created a transgenic mouse model that simulates aplastic anaemia in humans. The model shows the link between telomere impairment and bone marrow failure.
Researchers have identified an experimental drug, GSIs, that blocks Notch and prevents lung cancer growth in mice without treatment-related side effects. This discovery brings new clues for the treatment of lung cancer and is being tested in co-clinical trials.
A new strategy for treating aggressive skin cancer involves inducing cell differentiation to prevent tumor growth. Researchers identified a molecular mechanism that promotes the disappearance and inhibition of skin squamous cell carcinoma development.
Researchers at CNIO discover chimeric RNA, which combines information from multiple genes, and identify 175 transcripts and 12 new proteins. The study challenges the classical vision of genome storage and raises questions about the function and importance of this process.
A recent study published in Nature Genetics provides evidence that genetic variations in the embryo may predispose individuals to cancer later in life. The study found that mutations in key genes were present in cells of patients with congenital skin lesions, suggesting an early origin for some tumors.
Researchers at CNIO successfully test first gene therapy to combat aging, extending mouse lifespan up to 24 percent and improving health. The therapy delivers a 'rejuvenating' effect using telomerase enzyme, repairing or delaying DNA damage.
Researchers at CNIO have discovered a new target for developing anti-angiogenic and anti-tumoral therapies. The protein ephrinB2 was found to play a crucial role in angiogenesis and lymphoangiogenesis, processes that promote tumour growth and metastasis.
Researchers identified new functions of cohesin SA1 relevant to human disease, including efficient chromosome duplication and regulation of gene expression during embryonic development. This work offers new clues to understand the pathologies observed in CdLS patients and may lead to a better understanding of cancer.
Researchers created transgenic mice with light-emitting lymphatic vessels to study tumor cell dissemination. The technique detects lymph node invasion by tumor cells, providing a unique tool for studying inflammation and metastasis.
Researchers analyzed 100,000 molecular components from a patient's genome, revealing genetic risks and biomarkers for diseases. The study provides insights into the correlation between individual genetic profiles and environmental interactions in disease development.
Scientists have identified a paradoxical function of the gene Chk1, which is typically known for its anti-cancer properties. In this study, researchers found that extra copies of Chk1 actually facilitate tumor growth in mice, highlighting the complex role of this gene.
Researchers found that an anti-cancer gene can help combat obesity and age-related diseases by activating brown fat, a type of tissue that burns off excess fat. A synthetic compound with the same effect has been developed, offering hope for a new drug to boost tumour suppressors or improve nutrient metabolism.