Results 101 to 110 of about 424,553 (315)

Network divergence analysis identifies adaptive gene modules and two orthogonal vulnerability axes in pancreatic cancer

open access: yesMolecular Oncology, EarlyView.
Tumors contain diverse cellular states whose behavior is shaped by context‐dependent gene coordination. By comparing gene–gene relationships across biological contexts, we identify adaptive transcriptional modules that reorganize into distinct vulnerability axes.
Brian Nelson   +9 more
wiley   +1 more source

From Pathogenesis to Treatment: Targeting Type-2 Inflammation in Eosinophilic Esophagitis

open access: yesBiomolecules
Eosinophilic esophagitis (EoE) is a chronic inflammatory disorder of the esophagus. EoE shares a common pathogenetic mechanism with other chronic disorders pertaining to the type 2 inflammatory spectrum, such as atopic dermatitis (AD), allergic rhinitis (
Alberto Barchi   +11 more
doaj   +1 more source

RIPK4 function interferes with melanoma cell adhesion and metastasis

open access: yesMolecular Oncology, EarlyView.
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

COMP–PMEPA1 axis promotes epithelial‐to‐mesenchymal transition in breast cancer cells

open access: yesMolecular Oncology, EarlyView.
This study reveals that cartilage oligomeric matrix protein (COMP) promotes epithelial‐to‐mesenchymal transition (EMT) in breast cancer. We identify PMEPA1 (protein TMEPAI) as a novel COMP‐binding partner that mediates EMT via binding to the TSP domains of COMP, establishing the COMP–PMEPA1 axis as a key EMT driver in breast cancer.
Konstantinos S. Papadakos   +6 more
wiley   +1 more source

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

Cell motility influences microfluidics capturing in scRNA-seq [PDF]

open access: gold
Lara López-Escobar   +2 more
openalex   +1 more source

Use of polyvinylpyrrolidone and hyaluronic acid as sperm slower agent to compare recovery rate, motility rate, and viability of spermatozoa post thawing

open access: green, 2022
Haris Cakrasana   +5 more
openalex   +1 more source

Neurogastroenterology and Motility gets younger! [PDF]

open access: bronze, 2023
Maura Corsetti   +7 more
openalex   +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

Home - About - Disclaimer - Privacy