Results 131 to 140 of about 1,204,389 (301)
RIPK4 function interferes with melanoma cell adhesion and metastasis
RIPK4 promotes melanoma growth and spread. RIPK4 levels increase as skin lesions progress to melanoma. CRISPR/Cas9‐mediated deletion of RIPK4 causes melanoma cells to form less compact spheroids, reduces their migratory and invasive abilities and limits tumour growth and dissemination in mouse models.
Norbert Wronski +9 more
wiley +1 more source
RAD18 O-GlcNAcylation promotes translesion DNA synthesis and homologous recombination repair
RAD18, an important ubiquitin E3 ligase, plays a dual role in translesion DNA synthesis (TLS) and homologous recombination (HR) repair. However, whether and how the regulatory mechanism of O-linked N-acetylglucosamine (O-GlcNAc) modification governing ...
Xiaolu Ma +13 more
doaj +1 more source
The clinical use of the DNA damaging anticancer drug doxorubicin (DOX) is limited by irreversible cardiotoxicity, which depends on the cumulative dose.
Pelin Kücük +4 more
doaj +1 more source
Pre‐analytical handling critically determines liquid biopsy performance. This study defines practical best‐practice conditions for cell‐free DNA (cfDNA) and extracellular vesicle–derived DNA (evDNA), showing how processing time, storage conditions, tube type, and plasma input volume affect DNA integrity and mutation detection.
Jonas Dohmen +11 more
wiley +1 more source
Cytarabine is a key therapy for acute myeloid leukaemia (AML), but its efficacy is limited by the dNTPase SAMHD1, which hydrolyses its active metabolite. Screening nucleotide biosynthesis inhibitors revealed that IMPDH inhibitors selectively sensitise SAMHD1‐proficient AML cells to cytarabine.
Miriam Yagüe‐Capilla +9 more
wiley +1 more source
Keratin 19 (KRT19) is overexpressed in high‐grade serous ovarian cancer with high levels of Kallikrein‐related peptidases (KLK) 4–7 and is associated with poor survival. In vivo analyses demonstrate that elevated KRT19 increases peritoneal tumour burden.
Sophia Bielesch +13 more
wiley +1 more source
Somatic mutational landscape in von Hippel–Lindau familial hemangioblastoma
The causes of central nervous system (CNS) hemangioblastoma in Von Hippel–Lindau (vHL) disease are unclear. We used Whole Exome Sequencing (WES) on familial hemangioblastoma to investigate events that underlie tumor development. Our findings suggest that VHL loss creates a permissive environment for tumor formation, while additional alterations ...
Maja Dembic +5 more
wiley +1 more source
Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer
Dysregulation of the Hippo pathway drives nuclear accumulation of YAP/TAZ, activating stemness‐related transcriptional programs that sustain breast cancer stemness and fuel therapeutic resistance across subtypes, underscoring Hippo signaling as a targetable vulnerability. Figure created and edited with BioRender.com.
Giulia Schiavoni +11 more
wiley +1 more source
Senataxin, defective in ataxia oculomotor apraxia type 2, is involved in the defense against oxidative DNA damage. [PDF]
A defective response to DNA damage is observed in several human autosomal recessive ataxias with oculomotor apraxia, including ataxia-telangiectasia. We report that senataxin, defective in ataxia oculomotor apraxia (AOA) type 2, is a nuclear protein ...
BECHEREL OJ +13 more
core
E2A selectively regulates TGF‐β–induced apoptosis in KRAS‐mutant non‐small cell lung cancer
Ability to induce apoptosis by TGF‐β is frequently lost in advanced lung adenocarcinoma despite intact TGF‐β signaling. We identify E2A as a mutant KRAS–dependent mediator of resistance to TGF‐β–induced apoptosis. TGF‐β induces E2A via SMAD3 in mutant KRAS cells, and E2A silencing restores apoptosis and enhances radiation response in cell lines ...
Sergei Chuikov +3 more
wiley +1 more source

