Results 111 to 120 of about 573,279 (226)

Therapeutic applications of a novel humanized monoclonal antibody targeting chemokine receptor CCR9 in pancreatic cancer

open access: yesMolecular Oncology, EarlyView.
C–C chemokine receptor type 9 (CCR9) is an immune checkpoint in pancreatic ductal adenocarcinoma (PDAC). Novel anti‐CCR9 antibody SRB2 was evaluated in combination with cytotoxic chemotherapy in PDAC cells, patient‐derived organoids, patient‐derived xenografts, and humanized mouse models.
Hannah G. McDonald   +18 more
wiley   +1 more source

Interoperability between central counterparties [PDF]

open access: yes
In reaction to recent requests for interoperability between central counterparties of European stock markets, regulators have issued new guidelines to contain systemic risk. Our analysis confirms that the currently applied cross-CCP risk management model
Jürg Mägerle, Thomas Nellen
core  

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

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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