Results 191 to 200 of about 35,963,549 (224)
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
Trends in academic research on thirdhand smoke using bibliometric analysis. [PDF]
Ahialey JK, Lee Y, Park MB, Huh J.
europepmc +1 more source
Loss of the frequently mutated chromatin remodeler ARID1A, a subunit of the SWI/SNF cBAF complex, results in less open chromatin, alternative splicing, and the failure to stop cells from progressing through the cell cycle after DNA damage in bladder (cancer) cells. Created in BioRender. Epigenetic regulators, such as the SWI/SNF complex, with important
Rebecca M. Schlösser+11 more
wiley +1 more source
April, 1 \u2013 in the aftermath of elections: some words about the parliamentary majority [PDF]
Research, Update
core
A two-decade bibliometric analysis of drug resistance in oral cancer research: patterns, trends, and future directions. [PDF]
Xu X, Wang Z.
europepmc +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
Stress Among Research Scholars: Causes, Coping Strategies and Implications for Policy Reform. [PDF]
Kumar S, Singh G, Kumar A, Giri SK.
europepmc +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