Results 171 to 180 of about 2,114,568 (336)
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
HETEROGENEOUS CHARACTER OF STREPTOMYCIN-DEPENDENT MUTANTS OF A MYCOBACTERIUM [PDF]
Dirán Yegian, Vera Budd
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
COMPARATIVE STUDY OFESCHERICHIA COLIPHAGE T1 AND A PLAQUE TYPE MUTANT [PDF]
Ruth F. Hill
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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
STUDIES OF A PURINE- OR HISTIDINE-REQUIRING MUTANT OF ESCHERICHIA COLI
D. Luzzati, Robert Guthrie
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Human cytomegalovirus infection is common in normal prostate epithelium, prostate tumor tissue, and prostate cancer cell lines. CMV promotes cell survival, proliferation, and androgen receptor signaling. Anti‐CMV pharmaceutical compounds in clinical use inhibited cell expansion in prostate cancer models in vitro and in vivo, motivating investigation ...
Johanna Classon+13 more
wiley +1 more source
Elimination of Chromosomes Due to a Mutant (Minute-N) in Drosophila Melanogaster [PDF]
Calvin B. Bridges
openalex +1 more source
In luminal (ER+) breast carcinoma (BC), miRNA profiling identified miR‐195‐5p as a key regulator of proliferation that targets CHEK1, CDC25A, and CCNE1. High CHEK1 expression correlates with worse relapse‐free survival after chemotherapy, especially in patients with luminal A subtype.
Veronika Boušková+14 more
wiley +1 more source