Results 81 to 90 of about 552,030 (268)
Glycosylation in Intestinal Epithelium
, 1991 This chapter reviews the glycosylation reactions in the intestinal epithelium. The intestinal epithelium represents a good model system in which the glycosylation process can be studied. The intestinal epithelium is composed of two basic epithelial cell types: the absorptive enterocyte and the mucus-producing goblet cell.
Taatjes DJ, Roth J
openaire +4 more sources
Regulation of interleukin 33/ST2 signaling of human corneal epithelium in allergic diseases
International Journal of Ophthalmology, 2013 AIM: To identify the function of ST2 and explore the role of IL-33/ST2 signaling in regulating the pro-allergic cytokine production in human corneal epithelial cells (HCECs).METHODS: Human corneal tissues and cultured primary HCECs were treated with IL ...
Jing Lin
doaj +1 more source
Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer
Molecular Oncology, EarlyView.Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley +1 more source
Understanding the roles of gingival beta-defensins
Journal of Oral Microbiology, 2012 Gingival epithelium produces β-defensins, small cationic peptides, as part of its contribution to the innate host defense against the bacterial challenge that is constantly present in the oral cavity.
Ulvi Kahraman Gursoy +1 more
doaj +1 more source
Molecular Oncology, EarlyView.CIN85 is highly expressed in osteosarcoma, particularly in metastatic lesions. Its overexpression increases cell migration and Matrigel invasion, while silencing CIN85 suppresses these behaviors. Transcriptome analysis shows that CIN85 regulates MMP2, COL3A1, and Akt/mTOR signaling. Targeting these pathways reverses CIN85‐induced motility, highlighting
Iryna Horak +10 more
wiley +1 more source
Molecular Oncology, EarlyView.Circulating tumor cells (CTCs) and plasma cell‐free DNA (cfDNA) were analyzed to detect ESR1 mutations and methylation in patients with advanced breast cancer. CTC‐derived DNA showed higher sensitivity for mutation detection and revealed complementary genetic and epigenetic alterations, highlighting the added value of CTC analysis for understanding ...
Dimitra Stergiopoulou +12 more
wiley +1 more source
Molecular Oncology, EarlyView.Dormant cancer cells can hide in distant organs for years, evading treatment and the immune system. This review highlights how signals from the surrounding tissue and immune environment keep these cells inactive or trigger their reawakening. Understanding these mechanisms may help develop therapies to eliminate or control dormant cells and prevent ...
Kanishka Tiwary +1 more
wiley +1 more source
Molecular Oncology, EarlyView.Radiotherapy (RT) response depends on the DNA repair capacity of tumor and host cells. We show that circulating tumor cell (CTC) counts and apoptosis rates before and after RT predict treatment response and outcome, which can be accessed via easily accessible liquid biopsy approaches. Created in BioRender. Wikman, H.
Yvonne Goy +10 more
wiley +1 more source
Molecular Oncology, EarlyView.This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska +13 more
wiley +1 more source
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
Molecular Oncology, EarlyView.IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis +3 more
wiley +1 more source