Results 171 to 180 of about 11,284,305 (321)
TGF‐β has a complex role in cancer, exhibiting both tumor‐suppressive and tumor‐promoting properties. Using a series of differentiated tumoroids, derived from different stages and mutational background of colorectal cancer patients, we replicate this duality of TGF‐β in vitro. Notably, the atypical but highly aggressive KRASQ22K mutation rendered early‐
Theresia Mair+17 more
wiley +1 more source
Germline variants in CDKN2A wild‐type melanoma prone families
Among melanoma‐prone families, wild‐type for CDKN2A and CDK4, some have pathogenic variants in genes not usually linked to melanoma. Furthermore, rare XP‐related variants and variants in MC1R are enriched in such families. Germline pathogenic variants in CDKN2A are well established as an underlying cause of familial malignant melanoma. While pathogenic
Gjertrud T. Iversen+5 more
wiley +1 more source
Business in the information age: Heading for new processes [PDF]
Hubert Österle
openalex +1 more source
Chronic TGF‐β exposure drives epithelial HCC cells from a senescent state to a TGF‐β resistant mesenchymal phenotype. This transition is characterized by the loss of Smad3‐mediated signaling, escape from senescence, enhanced invasiveness and metastatic potential, and upregulation of key resistance modulators such as MARK1 and GRM8, ultimately promoting
Minenur Kalyoncu+11 more
wiley +1 more source
Language Lab Renovation Basics in the Age of Information [PDF]
Evans, Gilda A., Gibson, Anne L.
core +2 more sources
We identified adaptor protein ShcD as upregulated in triple‐negative breast cancer and found its expression to be correlated with reduced patient survival and increased invasion in cell models. Using a proteomic screen, we identified novel ShcD binding partners involved in EGFR signaling pathways.
Hayley R. Lau+11 more
wiley +1 more source
This article advocates integrating temporal dynamics into cancer research. Rather than relying on static snapshots, researchers should increasingly consider adopting dynamic methods—such as live imaging, temporal omics, and liquid biopsies—to track how tumors evolve over time.
Gautier Follain+3 more
wiley +1 more source
Alectinib resistance in ALK+ NSCLC depends on treatment sequence and EML4‐ALK variants. Variant 1 exhibited off‐target resistance after first‐line treatment, while variant 3 and later lines favored on‐target mutations. Early resistance involved off‐target alterations, like MET and NF2, while on‐target mutations emerged with prolonged therapy.
Jie Hu+11 more
wiley +1 more source