Results 131 to 140 of about 10,775,309 (319)

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

PSYCOLOGICAL AND PEDAGOGICAL ASPECTS OF USING COMPUTER SIMULATION IN TEACHING OF PLANNING AND ANALYSIS OF THE EXPERIMENT

open access: yesÌнформаційні технології в освіті, 2013
The article is devoted to the problem of increase the effectiveness of teaching students of planning and analysis of the experiment using the possibilities of computer simulation: experiments with the finished process models, special computer simulation ...
A. Rackovych
doaj  

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

An experiment on the use of disposable plastics as a reinforcement in concrete beams [PDF]

open access: yes
Illustrated here is the concept of reinforced concrete structures by the use of computer simulation and an inexpensive hands-on design experiment.
Chowdhury, Mostafiz R.
core   +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

PYCR1 inhibition in bone marrow stromal cells enhances bortezomib sensitivity in multiple myeloma cells by altering their metabolism

open access: yesMolecular Oncology, EarlyView.
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert   +13 more
wiley   +1 more source

Gentzen-Prawitz Natural Deduction as a Teaching Tool

open access: yes, 2009
We report a four-years experiment in teaching reasoning to undergraduate students, ranging from weak to gifted, using Gentzen-Prawitz's style natural deduction.
Ene, Cristian   +2 more
core   +1 more source

In vitro properties of patient serum predict clinical outcome after high dose rate brachytherapy of hepatocellular carcinoma

open access: yesMolecular Oncology, EarlyView.
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

open access: yesMolecular Oncology, EarlyView.
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

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

open access: yesMolecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak   +8 more
wiley   +1 more source

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