Results 91 to 100 of about 5,549,734 (191)
Molecular Oncology, EarlyView.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
YAP1::TFE3 mediates endothelial‐to‐mesenchymal plasticity in epithelioid hemangioendothelioma
Molecular 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
From Barcelona Process to Neighbourhood Policy: Assessments and Open Issues. CEPS Working Documents No. 220, 1 March 2005 [PDF]
, 2005 The Barcelona process so far has been a valuable systemic/institutional advance in Euro-Med relations and a confidence-building measure on a large scale. But it has not been a sufficient driving force to have created a momentum of economic, political and
Emerson, Michael, Noutcheva, Gergana.
core
Emerging role of ARHGAP29 in melanoma cell phenotype switching
Molecular 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
Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids
Molecular 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
Molecular 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
Molecular 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
Capital Collaboration: An In-Depth Look at the Community Investment System in Massachusetts Working Cities [PDF]
, 2016 This publication presents the work of the Capital & Collaboration Initiative, a cross-sector effort designed to increase the scale, efficiency and impact of investments in Massachusetts cities of more than 35,000 people (excluding Boston), characterized ...
Katie Grace, Robin Hacke
core
A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression
Molecular 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
Molecular Oncology, EarlyView.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