Results 101 to 110 of about 2,738,593 (315)
This study indicates that Merkel cell carcinoma (MCC) does not originate from Merkel cells, and identifies gene, protein & cellular expression of immune‐linked and neuroendocrine markers in primary and metastatic Merkel cell carcinoma (MCC) tumor samples, linked to Merkel cell polyomavirus (MCPyV) status, with enrichment of B‐cell and other immune cell
Richie Jeremian +10 more
wiley +1 more source
Hua-Bin Peng,1 Ying Liu,1 Fei Hou,1 Shuang Zhao,1 Yi-Zhi Zhang,1 Zhi-Ying He,1 Ting-Ting Cui,1 Jing-Yi Liu,1 Hao-Feng Xiong,1 Li-Ying Sun1– 5 1Department of Critical Liver Diseases, National Clinical Research Center for Digestive Diseases, Beijing ...
Peng HB +9 more
doaj
Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids
This study developed iPSC‐derived human liver organoids with TP53 gene knockout to model human liver fibrosis. These organoids showed elevated myofibroblast activation, early disease markers, and advanced fibrotic hallmarks. The use of profibrotic differentiation medium further amplified the fibrotic signature seen in the organoids.
Mustafa Karabicici +8 more
wiley +1 more source
Following high dose rate brachytherapy (HDR‐BT) for hepatocellular carcinoma (HCC), patients were classified as responders and nonresponders. Post‐therapy serum induced increased BrdU incorporation and Cyclin E expression of Huh7 and HepG2 cells in nonresponders, but decreased levels in responders.
Lukas Salvermoser +14 more
wiley +1 more source
Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu +18 more
wiley +1 more source
Pattern of liver function and clinical profile in COVID-19: A cross-sectional study of 91 patients
Abhishek Kumar +5 more
openalex +2 more sources
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié +16 more
wiley +1 more source
Background Due to its well-established involvement in clot formation, von Willebrand factor (vWF) has been held responsible for decades as a risk factor for arterio-venous thrombosis. It is currently unclear how genetic differences in vWF genes relate to
Isis Samy Bedira +6 more
doaj +1 more source

