Results 221 to 230 of about 1,934,866 (340)

Hypomethylating agents increase L1 retroelement expression without inducing novel insertions in myeloid malignancies

open access: yesMolecular Oncology, EarlyView.
We investigated whether hypomethylating agents (HMAs) used in myeloid malignancies induce somatic retrotransposition. Our findings indicate that HMA treatment increases L1‐encoded protein expression but does not lead to detectable de novo retrotransposition events in either patient samples or cell lines.
Šárka Pavlová   +14 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

SensRORing cholesterol to drive protumoral myelopoiesis

open access: yesMolecular Oncology, EarlyView.
Bleve et al. uncover a cholesterol‐driven immune evasion pathway, where RORγ‐dependent myelopoiesis shapes tumor immunosuppression. Targeting RORγ and PCSK9 emerges as a strategy to boost cancer immunotherapy. Protumoral myelopoiesis is a determinant of immunoevasion and tumor spread in many malignancies.
Sara Gennari, Luigi Nezi, Teresa Manzo
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

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