Results 151 to 160 of about 2,545,958 (345)

Thalassemia: genotypes and phenotypes

open access: yesAnnals of Hematology, 1991
The large degree of phenotypic heterogeneity of thalassemia can now be related to the underlying genomic defects. This information has accumulated rapidly over the last years through the recent advances in molecular technology. The list of main types of thalassemia (alpha or beta) that can be differentiated includes several gene deletions (complete or ...
openaire   +6 more sources

The influence of ROS1 fusion partners and resistance mechanisms in ROS1‐TKI‐treated non‐small cell lung cancer patients

open access: yesMolecular Oncology, EarlyView.
This real‐world study of ROS1+ NSCLC highlights fusion diversity, treatment outcomes with crizotinib and lorlatinib, and in vitro experiments with resistance mechanisms. G2032R drives strong resistance to ROS1‐targeted TKIs, especially lorlatinib. Fusion partner location does not affect overall survival to crizotinib or lorlatinib. Findings support the
Fenneke Zwierenga   +8 more
wiley   +1 more source

YAP1::TFE3 mediates endothelial‐to‐mesenchymal plasticity in epithelioid hemangioendothelioma

open access: yesMolecular Oncology, EarlyView.
The YAP1::TFE3 fusion protein drives endothelial‐to‐mesenchymal transition (EndMT) plasticity, resulting in the loss of endothelial characteristics and gain of mesenchymal‐like properties, including resistance to anoikis, increased migratory capacity, and loss of contact growth inhibition in endothelial cells.
Ant Murphy   +9 more
wiley   +1 more source

Emerging role of ARHGAP29 in melanoma cell phenotype switching

open access: yesMolecular Oncology, EarlyView.
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster   +3 more
wiley   +1 more source

Two Further Serum Pseudocholinesterase Phenotypes as Causes of Suxamethonium Apnoea [PDF]

open access: green, 1963
H. Lehmann   +4 more
openalex   +1 more source

Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids

open access: yesMolecular Oncology, EarlyView.
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

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