Results 41 to 50 of about 46,139 (228)
Aggressive prostate cancer is associated with pericyte dysfunction
Tumor‐produced TGF‐β drives pericyte dysfunction in prostate cancer. This dysfunction is characterized by downregulation of some canonical pericyte markers (i.e., DES, CSPG4, and ACTA2) while maintaining the expression of others (i.e., PDGFRB, NOTCH3, and RGS5).
Anabel Martinez‐Romero +11 more
wiley +1 more source
Survivin and Aurora Kinase A control cell fate decisions during mitosis
Aurora A interacts with survivin during mitosis and regulates its centromeric role. Loss of Aurora A activity mislocalises survivin, the CPC and BubR1, leading to disruption of the spindle checkpoint and triggering premature mitotic exit, which we refer to as ‘mitotic slippage’.
Hana Abdelkabir +2 more
wiley +1 more source
Liquid biopsy epigenetics: establishing a molecular profile based on cell‐free DNA
Cell‐free DNA (cfDNA) fragments in plasma from cancer patients carry epigenetic signatures reflecting their cells of origin. These epigenetic features include DNA methylation, nucleosome modifications, and variations in fragmentation. This review describes the biological properties of each feature and explores optimal strategies for harnessing cfDNA ...
Christoffer Trier Maansson +2 more
wiley +1 more source
Combining PTEN protein assessment and transcriptomic profiling of prostate tumors, we uncovered a network enriched in senescence and extracellular matrix (ECM) programs associated with PTEN loss and conserved in a mouse model. We show that PTEN‐deficient cells trigger paracrine remodeling of the surrounding stroma and this information could help ...
Ivana Rondon‐Lorefice +16 more
wiley +1 more source
Defective α-galactosidase A (AGAL/GLA) due to missense or nonsense mutations in the GLA gene results in accumulation of the glycosphingolipids globotriaosylceramide (Gb3) and its deacylated derivate globotriaosylsphingosine (lyso-Gb3) in cells and body fluids.
Björn Laffer +6 more
openaire +3 more sources
Potential therapeutic targeting of BKCa channels in glioblastoma treatment
This review summarizes current insights into the role of BKCa and mitoBKCa channels in glioblastoma biology, their potential classification as oncochannels, and the emerging pharmacological strategies targeting these channels, emphasizing the translational challenges in developing BKCa‐directed therapies for glioblastoma treatment.
Kamila Maliszewska‐Olejniczak +4 more
wiley +1 more source
ATF4‐mediated stress response as a therapeutic vulnerability in chordoma
We screened 5 chordoma cell lines against 100+ inhibitors of epigenetic and metabolic pathways and kinases and identified halofuginone, a tRNA synthetase inhibitor. Mechanistically halofuginone induces an integrated stress response, with eIF2alpha phosphorylation, activation of ATF4 and its target genes CHOP, ASNS, INHBE leading to cell death ...
Lucia Cottone +11 more
wiley +1 more source
Peroxidasin enables melanoma immune escape by inhibiting natural killer cell cytotoxicity
Peroxidasin (PXDN) is secreted by melanoma cells and binds the NK cell receptor NKG2D, thereby suppressing NK cell activation and cytotoxicity. PXDN depletion restores NKG2D signaling and enables effective NK cell–mediated melanoma killing. These findings identify PXDN as a previously unrecognized immune evasion factor and a potential target to improve
Hsu‐Min Sung +17 more
wiley +1 more source
Redox regulation meets metabolism: targeting PRDX2 to prevent hepatocellular carcinoma
PRDX2 acts as a central redox hub linking metabolic dysfunction‐associated steatohepatitis (MASH) to hepatocellular carcinoma (HCC). In normal hepatocytes, PRDX2 maintains redox balance and metabolic homeostasis under oxidative stress. In contrast, during malignant transformation, PRDX2 promotes oncogenic signaling, stemness, and tumor initiation ...
Naroa Goikoetxea‐Usandizaga +2 more
wiley +1 more source
This work identified serum proteins associated with pancreatic epithelial neoplasms (PanINs) and early‐stage PDAC. Proteomics screens assessed genetically engineered mice with abundant PanINs, KPC mice (Lox‐STOP‐Lox‐KrasG12D/+ Lox‐STOP‐Lox‐Trp53R172H/+ Pdx1‐Cre) before PDAC development and also early‐stage PDAC patients (n = 31), compared to benign ...
Hannah Mearns +10 more
wiley +1 more source

