Results 121 to 130 of about 594,928 (357)

ITGAV and SMAD4 influence the progression and clinical outcome of pancreatic ductal adenocarcinoma

open access: yesMolecular Oncology, EarlyView.
In SMAD4‐positive pancreatic ductal adenocarcinoma (PDAC), integrin subunit alpha V (ITGAV) activates latent TGF‐β, which binds to the TGF‐β receptor and phosphorylates SMAD2/3. The activated SMAD2/3 forms a complex with SMAD4, and together they translocate to the nucleus, modulating gene expression to promote proliferation, migration, and invasion. In
Daniel K. C. Lee   +9 more
wiley   +1 more source

Co-Evolution of quasispecies: B-cell mutation rates maximize viral error catastrophes

open access: yes, 2001
Co-evolution of two coupled quasispecies is studied, motivated by the competition between viral evolution and adapting immune response. In this co-adaptive model, besides the classical error catastrophe for high virus mutation rates, a second ...
A. Aigner   +29 more
core   +1 more source

β‐TrCP overexpression enhances cisplatin sensitivity by depleting BRCA1

open access: yesMolecular Oncology, EarlyView.
Low levels of β‐TrCP (Panel A) allow the accumulation of BRCA1 and CtIP, which facilitate the repair of cisplatin‐induced DNA damage via homologous recombination (HR) and promote tumor cell survival. In contrast, high β‐TrCP expression (Panel B) leads to BRCA1 and CtIP degradation, impairing HR repair, resulting in persistent DNA damage and apoptosis ...
Rocío Jiménez‐Guerrero   +8 more
wiley   +1 more source

Begomovirus quasispecies adapt to hosts by exploring different sequence space without changing their consensus sequences [PDF]

open access: yes, 2014
Geminiviruses possess single-stranded circular DNA genomes that depend on cellular polymerases for replication in the host nucleus. In plant hosts, geminivirus populations behave as ensembles of mutant and recombinant genomes.
Domínguez-Huerta, Guillermo   +5 more
core  

Unveiling unique protein and phosphorylation signatures in lung adenocarcinomas with and without ALK, EGFR, and KRAS genetic alterations

open access: yesMolecular Oncology, EarlyView.
Proteomic and phosphoproteomic analyses were performed on lung adenocarcinoma (LUAD) tumors with EGFR, KRAS, or EML4–ALK alterations and wild‐type cases. Distinct protein expression and phosphorylation patterns were identified, especially in EGFR‐mutated tumors. Key altered pathways included vesicle transport and RNA splicing.
Fanni Bugyi   +12 more
wiley   +1 more source

RKIP overexpression reduces lung adenocarcinoma aggressiveness and sensitizes cells to EGFR‐targeted therapies

open access: yesMolecular Oncology, EarlyView.
RKIP, a metastasis suppressor protein, modulates key oncogenic pathways in lung adenocarcinoma. In silico analyses linked low RKIP expression to poor survival. Functional studies revealed RKIP overexpression reduces tumor aggressiveness and enhances sensitivity to EGFR‐targeted therapies, while its loss promotes resistance.
Ana Raquel‐Cunha   +10 more
wiley   +1 more source

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

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

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