Results 121 to 130 of about 2,417,970 (339)
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
TRIM24 and TRIM28 are androgen receptor (AR) coregulators which exhibit increased expression with cancer progression. Both TRIM24 and TRIM28 combine to influence the response of castrate‐resistant prostate cancer (CRPC) cells to AR inhibitors by mediating AR signalling, regulation of MYC and upregulating VEGF to promote angiogenesis. Castrate‐resistant
Damien A. Leach+8 more
wiley +1 more source
EMT‐associated bias in the Parsortix® system observed with pancreatic cancer cell lines
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
Identificaram-se diferenciais geográficos e socioeconômicos do padrão de qualidade da informação sobre a causa básica de morte dos idosos no Brasil.
Solange Kanso+3 more
doaj
Normally Unequal Growth as a Possible Cause of Death [PDF]
Frank E. Beddard
openalex +1 more source
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
THE FULMINATING TYPE OF CEREBROSPINAL FEVER: PATHOLOGY, AND CAUSE OF DEATH [PDF]
Patrick Maclagan, W. E. Cooke
openalex +1 more source
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