Results 41 to 50 of about 10,701 (149)
Tyrosine kinase inhibitors (TKIs) targeting epidermal growth factor receptor (EGFR) protein serve as a critical pillar in the treatment of non-small cell lung cancer (NSCLC), but resistance is universal.
Jiahui Wu +6 more
doaj +1 more source
CADASIL syndrome in a large Turkish kindred caused by the R90C mutation in the Notch3 receptor
Mutations in the Notch3 gene are the cause of the autosomal dominant disorder CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy). The CADASIL is an adult‐onset neurologic disorder (average age of onset is 45 years) characterized by recurrent strokes and dementia. Clinical features combined with cerebral
Utku, U +4 more
openaire +3 more sources
The NOTCH3 Downstream Target HEYL Is Required for Efficient Human Airway Basal Cell Differentiation
Basal cells (BCs) are stem/progenitor cells of the mucociliary airway epithelium, and their differentiation is orchestrated by the NOTCH signaling pathway.
Manish Bodas +8 more
doaj +1 more source
Human clinically non-functioning pituitary adenomas (NFPAs) primarily cause headaches, visual impairment and hypopituitarism due to the effect of the mass of the tumor. Surgery is the first-line treatment for these tumors. To date, no efficacious medical therapy exists for non-functioning adenomas.
LU, RUNCHUN +5 more
openaire +3 more sources
Sepsis downregulates aortic Notch signaling to produce vascular hyporeactivity in mice
Inhibition of Notch signaling in macrophages is known to reduce inflammation, however, its role in regulating vascular hyporeactivity in sepsis is unknown. Thus we aimed to evaluate the effect of sepsis on vascular Notch signaling.
Vandana Singh +8 more
doaj +1 more source
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a inherited cerebral small vessel disease caused by Notch3 gene mutation. The molecular⁃genetic mechanisms of CADASIL have been still unclear.
SUN Yuan⁃jing, FAN Yu⁃hua
doaj +1 more source
Development of therapies targeting cancer‐associated fibroblasts (CAFs) necessitates preclinical model systems that faithfully represent CAF–tumor biology. We established an in vitro coculture system of patient‐derived pancreatic CAFs and tumor cell lines and demonstrated its recapitulation of primary CAF–tumor biology with single‐cell transcriptomics ...
Elysia Saputra +10 more
wiley +1 more source
Novel mechanism of resistance to targeted therapies in lung cancer
We have identified a non-canonical role of0 Notch3 in response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy, whereby Notch3 associates with β-catenin, resulting in increased catenin beta-1 (CTNNB1, best known as β ...
Walter Wang +2 more
doaj +1 more source
SUSD2 Promotes Metastasis and Primary Tumor Growth in Pancreatic Cancer Cells via Integrin-FAK Signaling Activation. [PDF]
This study investigates the role of Sushi domain‐containing 2 (SUSD2) in pancreatic ductal adenocarcinoma (PDAC) and demonstrates that SUSD2 enhances both metastasis and primary tumor growth by promoting integrin β1–FAK signaling. SUSD2 interacts with integrin β1, enhancing adhesion to extracellular matrix (ECM) components such as collagen 1 and ...
Yoshida J +11 more
europepmc +2 more sources
COMP–PMEPA1 axis promotes epithelial‐to‐mesenchymal transition in breast cancer cells
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

