Results 61 to 70 of about 1,312,581 (296)
Molecular Oncology, EarlyView.Loss of primary cilia in endothelial cells promotes EndMT and vascular abnormalities in the ovarian tumor microenvironment through EphA2 activation. Using human samples, in vitro models, and endothelial‐specific Kif3a‐knockout mice, we show that primary cilia loss drives the acquisition of cancer‐associated fibroblast‐like phenotypes, thereby ...
Jin Gu Cho +11 more
wiley +1 more source
Molecular 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
Molecular 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
Molecular 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
Acta Scientiae Veterinariae, 2016 Background: Congenital defects consist of structural or functional abnormalities present at birth, which partially or globally affect the systems. Among the defects are the conjoined twins, a rare congenital anomaly caused by fusion of two monozygotic embryos which can be classified according to the different sites of union.
dos Santos, Marilúcia Campos +6 more
openaire +4 more sources
Molecular 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
Molecular Oncology, EarlyView.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
Chimeric diphtheria toxin–CCL8 cytotoxic peptide for breast cancer management
Molecular Oncology, EarlyView.DTCCL8 is a recombinant fusion toxin that targets cancer cells expressing chemokine receptors. By combining diphtheria toxin with CCL8, DTCCL8 binds to multiple receptors on tumor cells and induces selective cytotoxicity. This strategy enables receptor‐mediated targeting of cancer and may support the development of chemokine‐guided therapeutics ...
Bernardo Chavez +5 more
wiley +1 more source
ITGAV and SMAD4 influence the progression and clinical outcome of pancreatic ductal adenocarcinoma
Molecular Oncology, EarlyView.In SMAD4‐positive pancreatic ductal adenocarcinoma (PDAC), integrin subunit alpha V (ITGAV) activates latent TGF‐β, which binds to the TGF‐β receptor and phosphorylates SMAD2/3. The activated SMAD2/3 forms a complex with SMAD4, and together they translocate to the nucleus, modulating gene expression to promote proliferation, migration, and invasion. In
Daniel K. C. Lee +9 more
wiley +1 more source