Results 161 to 170 of about 8,906,865 (345)

BMP antagonist CHRDL2 enhances the cancer stem‐cell phenotype and increases chemotherapy resistance in colorectal cancer

open access: yesMolecular Oncology, EarlyView.
Overexpression of CHRDL2 in colon cancer cells makes them more stem‐like and resistant to chemo‐ and radiotherapy. CHRDL2‐high cells have upregulation of the WNT pathway, genes involved in the DNA damage response (DDR) pathway and epithelial‐to‐mesenchymal transition (EMT). This leads to quicker repair of damaged DNA and more cell migration.
Eloise Clarkson, Annabelle Lewis
wiley   +1 more source

EMT‐associated bias in the Parsortix® system observed with pancreatic cancer cell lines

open access: yesMolecular Oncology, EarlyView.
The Parsortix® system was tested for CTC enrichment using pancreatic cancer cell lines with different EMT phenotypes. Spike‐in experiments showed lower recovery of mesenchymal‐like cells. This was confirmed with an EMT‐inducible breast cancer cell line.
Nele Vandenbussche   +8 more
wiley   +1 more source

Tumor clusters with divergent inflammation and human retroelement expression determine the clinical outcome of patients with serous ovarian cancer

open access: yesMolecular Oncology, EarlyView.
Analysis of treatment‐naïve high‐grade serous ovarian carcinoma (HGSOC) and control tissues for ERVs, LINE‐1 (L1), inflammation, and immune checkpoints identified five clusters with diverse patient recurrence‐free survivals. An inflammation score was calculated and correlated with retroelement expression, where one novel cluster (Triple‐I) with high ...
Laura Glossner   +6 more
wiley   +1 more source

Hacia la extensión de la responsabilidad para otros intermediarios en Internet

open access: yesRevista Iberoamericana de la Propiedad Intelectual, 2016
Cicerón, en su Defensa de Sexto Riscio Amerino señalaba: “El célebre Lucio Casio, a quien el pueblo romano tenía por juez concienzudo y experimentado, solía preguntar a menudo en las causas ‘quien había salido beneficiado’ [cui bono fuisset].
Ernesto Rengifo García
doaj  

EGFR‐STAT3 activation provides a therapeutic rationale for targeting aggressive ETV1‐positive prostate cancer

open access: yesMolecular Oncology, EarlyView.
Cotargeting EGFR and STAT3 with Erlotinib and TTI‐101 impairs both 2D and 3D growth of ETV1‐overexpressing prostate cancer cells by disrupting a self‐sustaining ETV1–EGFR positive feedback loop that promotes EGFR and STAT3 expression and phosphorylation (activation).
Elsa Gomes Paiva   +5 more
wiley   +1 more source

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