position-guided-nasopharyngeal-irrigation-for-post-radiotherapy-ulcer

Position-Guided Nasopharyngeal Irrigation for Post-Radiotherapy Ulcer Care in Nasopharyngeal Carcinoma

To describe and standardize a position-guided nasopharyngeal irrigation protocol for post-radiotherapy nasopharyngeal ulceration (RINU) in patients with ...

The First Affiliated Hospital of Hainan Medical University

 Bevacizumab is a recombinant humanized monoclonal antibody that blocks vascular endothelial growth factor (VEGF) with clear clinical benefits. However, overall survival of some cancer types remains low owing to resistance to bevacizumab therapy. While resistance is commonly ascribed to tumor cell invasion induced by hypoxia-inducible factor (HIF), less attention has been paid to the potential involvement of endothelial cells (ECs) in vasculature activated by anti-angiogenic drugs.  Human umbilical vein ECs (HUVECs), bEnd.3 cells, and mouse retinal microvascular ECs (MRMECs) were treated with bevacizumab under conditions of hypoxia and effects on biological behaviors, such as migration and tube formation, examined. Regulatory effects on TGFβ1 and CD105 (endoglin) were established  determination of protein and mRNA levels. We further investigated whether the effects of bevacizumab could be reversed using the receptor tyrosine kinase inhibitor anlotinib.  Bevacizumab upregulated TGFβ1 as well as CD105, a component of the TGFβ receptor complex and an angiogenesis promoter. Elevated CD105 induced activation of Smad1/5, the inflammatory pathway and endothelial-mesenchymal transition. The migration ability of HUVECs was enhanced by bevacizumab under hypoxia. Upregulation of CD105 was abrogated by anlotinib, which targets multiple receptor tyrosine kinases including VEGFR2/3, FGFR1-4, PDGFRα/β, C-Kit, and RET.  Bevacizumab promotes migration and tube formation of HUVECs  activation of the TGFβ1 pathway and upregulation of CD105 expression. Anlotinib reverses the effects of bevacizumab by inhibiting the above signals.

Bevacizumab promotes active biological behaviors of human umbilical vein endothelial cells by activating TGFβ1 pathways  off-VEGF signaling.

Circular RNAs (circRNAs) are closely associated with cancer pathogenesis. The purpose of our current study was to explore the role and mechanism of circ_0060967 in colorectal cancer (CRC) development.

Circ_0060967 contributes to colorectal cancer progression by sponging miR-1184 to up-regulate SRC proto-oncogene.

Insufficient radiofrequency ablation (IRFA) increases the risk of hepatocellular carcinoma (HCC) recurrence and metastasis. Our previous study revealed that IRFA downregulates FUNDC2P4 and promotes epithelial-mesenchymal transition (EMT), but the mechanisms remain unclear.

Mechanistic insights into FUNDC2P4 and HSF1 regulation of EMT in residual hepatocellular carcinoma following insufficient radiofrequency ablation.

Immune checkpoint inhibitors (ICIs) have been increasingly used in hepatocellular carcinoma (HCC). Despite emerging evidence indicating that concomitant medications might impact clinical outcomes, their association with ICI efficacy is undefined in HCC.

Article	Year
Bevacizumab promotes active biological behaviors of human umbilical vein endothelial cells by activating TGFβ1 pathways off-VEGF signaling. Cancer biology & medicine\| PubMed ID: 32587778	2020
Circ_0060967 contributes to colorectal cancer progression by sponging miR-1184 to up-regulate SRC proto-oncogene. Arab journal of gastroenterology : the official publication of the Pan-Arab Association of Gastroenterology\| PubMed ID: 37045727	2023
Mechanistic insights into FUNDC2P4 and HSF1 regulation of EMT in residual hepatocellular carcinoma following insufficient radiofrequency ablation. International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group\| PubMed ID: 40903993	2025
Concomitant medication use and clinical outcome in hepatocellular carcinoma treated with immune-based therapy: a multicenter analysis. Frontiers in immunology\| PubMed ID: 41394828	2025

Chengmou Huang

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