Results 111 to 120 of about 4,009,783 (237)

Engineered extracellular vesicles enriched with the miR‐214/199a cluster enhance the efficacy of chemotherapy in ovarian cancer

open access: yesMolecular Oncology, EarlyView.
Loss of the miR‐214/199a cluster is associated with recurrence in ovarian cancer. Engineered small extracellular vesicles (m214‐sEVs) elevate miR‐214‐3p/miR‐199a‐5p in tumor cells, suppress β‐catenin, TLR4, and YKT6 signaling, reprogram tumor‐derived sEV cargo, reduce chemoresistance and migration, and enhance carboplatin efficacy and survival in ...
Weida Wang   +12 more
wiley   +1 more source

Keratin 19 as a prognostic marker and contributing factor of metastasis and chemoresistance in high‐grade serous ovarian cancer

open access: yesMolecular Oncology, EarlyView.
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

Establishment of a humanized patient‐derived xenograft mouse model of high‐grade serous ovarian cancer for preclinical evaluation of combination immunotherapy

open access: yesMolecular Oncology, EarlyView.
We have established a humanized orthotopic patient‐derived xenograft (Hu‐oPDX) mouse model of high‐grade serous ovarian cancer (HGSOC) that recapitulates human tumor–immune interactions. Using combined anti‐PD‐L1/anti‐CD73 immunotherapy, we demonstrate the model's improved biological relevance and enhanced translational value for preclinical ...
Luka Tandaric   +10 more
wiley   +1 more source

E2A selectively regulates TGF‐β–induced apoptosis in KRAS‐mutant non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
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

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

open access: yesMolecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu   +10 more
wiley   +1 more source

Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

open access: yesMolecular Oncology, EarlyView.
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley   +1 more source

Overview of molecular signatures of senescence and associated resources: pros and cons

open access: yesFEBS Open Bio, EarlyView.
Cells can enter a stress response state termed cellular senescence that is involved in various diseases and aging. Detecting these cells is challenging due to the lack of universal biomarkers. This review presents the current state of senescence identification, from biomarkers to molecular signatures, compares tools and approaches, and highlights ...
Orestis A. Ntintas   +6 more
wiley   +1 more source

Targeting TNBC: core–shell polycationic polyurea dendrimers with inherent anticancer activity

open access: yesFEBS Open Bio, EarlyView.
Core–shell polycationic PURE dendrimers were tested in TNBC‐derived tumor models. Both formulations selectively targeted TNBC and effectively reduced tumor volume. PUREG4‐OEI48 suppressed tumor growth without detectable toxicity, whereas PUREG4‐OCEI24, despite showing efficacy, induced hepatic toxicity.
Adriana Cruz   +9 more
wiley   +1 more source

DDX3X induces mesenchymal transition of endothelial cells by disrupting BMPR2 signaling

open access: yesFEBS Open Bio, EarlyView.
Elevated DDX3X expression led to downregulation of BMPR2, a key regulator of endothelial homeostasis and function. Our co‐immunoprecipitation assays further demonstrated a molecular interaction between DDX3X and BMPR2. Notably, DDX3X promoted lysosomal degradation of BMPR2, thereby impairing its downstream signaling and facilitating endothelial‐to ...
Yu Zhang   +7 more
wiley   +1 more source

Nintedanib Lacks Efficacy in a Spirometry-Confirmed and Bleomycin-Induced Mouse Model of Idiopathic Pulmonary Fibrosis. [PDF]

open access: yesBasic Clin Pharmacol Toxicol
Bousamaki J   +12 more
europepmc   +1 more source

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