Results 211 to 220 of about 5,358,439 (388)

Crisis

open access: yes, 1958
Documento perteneciente al Legado Germán Bernácer. Artículo de prensa. Separata del artículo publicado en: Bernácer Tormo, G (1958) "Crisis", Información, 30 de septiembre, pp. 717-718 con ISSN 0212-8845.
openaire   +2 more sources

Nepal: Dangerous Plans for Village Militias [PDF]

open access: yes, 2004
International Crisis Group
core  

Investigating the cell of origin and novel molecular targets in Merkel cell carcinoma: a historic misnomer

open access: yesMolecular 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

Crisis

open access: yesJACC: Cardiovascular Interventions, 2009
openaire   +2 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

Nepal: Back to the Gun [PDF]

open access: yes, 2003
International Crisis Group
core  

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

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