In an isomerization reaction, uridine is modified to pseudouridine, the most abundant RNA modification which presents an extra hydrogen bond donor, altering the RNA structure and providing unique chemical properties.
Pancreatic cancer remains one of the deadliest cancers, with survival rates showing little improvement over decades and projections placing it as the second leading cause of cancer deaths by 2030. Chemotherapy is essential for all patients, yet most tumors lacking BRCA1/2 or PALB2 mutations show resistance to cisplatin. Growing evidence suggests that targeting nuclear factor NF-κB, a key driver of cancer progression, could help overcome this chemoresistance and improve treatment outcomes.
Glioblastoma multiforme (GBM) is the most aggressive and common type of brain cancer in adults, with a dismal prognosis despite current treatments. Previous work found that neurodevelopmental pathways drive glioma tumor initiation, maintenance and progression through fetal oncogenes, which are active in development and cancer but largely absent in adult tissues, offering precise therapeutic targets with minimal off-target effects.
Acute myeloid leukemia (AML) is an aggressive blood cancer with poor clinical outcomes and high mortality rates, primarily driven by drug resistance and relapse. Increasing evidence has confirmed dysregulated cellular metabolism as a tumor hallmark with crucial roles in tumor growth, progression and drug resistance.
Mutations that activate phosphorylation of certain Rab GTPases by LRRK2 have been linked to a subset of genetic cases of Parkinson’s disease, and PPM1M is one of the phosphatases responsible for reversing phosphorylation by LRRK2.
Immunoglobulin superfamily 11 (IgSF11) overexpression has been observed in several cancer types, including gastric cancer, hepatocellular carcinoma, colorectal cancers and gliomas, and linked to aggressive clinicopathological features. Therefore, IgSF11 has been proposed as a novel immune checkpoint ligand and a candidate for cancer immunotherapy. However, the potential role and clinical significance of IgSF11 in human breast cancer remain unexplored.
Barth syndrome is a rare genetic disorder caused by mutations in the TAZ gene, which encodes an enzyme essential for remodeling cardiolipin, critical for mitochondrial function. A recent study published in Nature identified the enzyme ABHD18 as a candidate deacylase in the cardiolipin biosynthesis pathway and a potential therapeutic target for this syndrome.
Metabolic dysfunction-associated steatotic liver disease (MASLD) now affects over a third of adults worldwide. Its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), is a leading driver of cirrhosis, cancer and liver transplants while often coexisting with diabetes, obesity and cardiovascular disease.
The mechanisms behind diabetic cardiomyopathy (DCM) have been deeply studied but still not well-established within the scientific community. Mutations in cardiac junction proteins may result in heart failure and arrhythmia. ER degradation enhancing α-mannosidase like protein 2 (EDEM2) is involved in the degradation of misfolded N-glycosylated proteins, but its role in the heart is not clear and was investigated.
Hypoxia is a common event in the microenvironment of solid tumors, triggering some changes in gene expression profiles to adapt to low-oxygen levels. Increasing evidence exists regarding hypoxia and mitochondrial dysfunction to play a role in the progression of non-small-cell lung cancer (NSCLC).
