Clinical trials using anti-vascular endothelial growth factor /(VEGF) molecules induce a modest improvement in overall survival, measurable in weeks to just a few months, and tumors respond differently to these agents. In this review article, we have exposed some tumor characteristics and processes that may impair the effectiveness of anti-angiogenic approaches, including genotypic changes on endothelial cells, the vascular normalization phenomenon, and the vasculogenic mimicry. The usage of anti-angiogenic molecules leads to hypoxic tumor microenvironment which enhances tumor invasiveness. The role of tumor-infiltrating cells, including tumor associated macrophages and fibroblasts (TAMs and TAFs) in the therapeutic response to anti-angiogenic settings was also highlighted. Finally, among the new therapeutic approaches to target tumor vasculature, anti-PD-1 or anti-PD-L1 therapy sensitizing and prolonging the efficacy of anti-angiogenic therapy, have been discussed.
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http://dx.doi.org/10.1016/j.tranon.2019.04.022 | DOI Listing |
Future Med Chem
January 2025
School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation, Yantai University, Yantai, China.
Biomark Med
January 2025
The Nutristasis Unit, Synnovis, St. Thomas' Hospital, London, UK.
This case describes a patient with pancreatic exocrine insufficiency and persistently elevated serum vitamin B12 concentrations that were not due to supplementation or associated with hepatic or hematological pathology. Laboratory investigations suggested the presence of macro-B12 as the cause of this patient's raised serum vitamin B12. Macro-B12 is often formed when vitamin B12-vitamin binding proteins (transcobalamin and haptocorrin) complex with immunoglobulins.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
Department of Neurology, Jinshan Hospital, Fudan University, 201508 Shanghai, China.
Background: Neuronal cholesterol deficiency may contribute to the synaptopathy observed in Alzheimer's disease (AD). However, the underlying mechanisms remain poorly understood. Intact synaptic vesicle (SV) mobility is crucial for normal synaptic function, whereas disrupted SV mobility can trigger the synaptopathy associated with AD.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
Department of Translational Medicine Center, The First Affiliated Hospital of Zhengzhou University, 450052 Zhengzhou, Henan, China.
Front Biosci (Landmark Ed)
January 2025
Department of Cardiothoracic Surgery, The Affiliated Jiangyin Hospital of Nantong University, 214400 Jiangyin, Jiangsu, China.
Background: This study investigates the role of small ubiquitin-like modifier (SUMO)-specific peptidase 5 (SENP5), a key regulator of SUMOylation, in esophageal squamous cell carcinoma (ESCC), a lethal disease, and its underlying molecular mechanisms.
Methods: Differentially expressed genes between ESCC mouse oesophageal cancer tissues and normal tissues were analysed via RNA-seq; among them, SENP5 expression was upregulated, and this gene was selected for further analysis. Immunohistochemistry and western blotting were then used to validate the increased protein level of SENP5 in both mouse and human ESCC samples.
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