ArticleJournal of translational medicine2024
EBV-induced upregulation of CD55 reduces the efficacy of cetuximab treatment in nasopharyngeal carcinoma.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed.
- Review
- EBV hijacks the metabolic function of CD73 to resist the antitumor function of NK cells.NPJ precision oncology · 2026Article
- Review
- Advances in immunotherapy and targeted therapy for nasopharyngeal carcinoma: Current progress and combined approaches (Review).Oncology reports · 2026Review
- Harnessing the immune microenvironment: advances in nasopharyngeal carcinoma immunotherapy.Cell death discovery · 2026Review
- Review
- Upregulated ARMCX1 suppresses nasopharyngeal carcinoma progression by promoting TRIM21-mediated β-catenin degradation.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Progress and prospects for herpesvirus vaccination using gB antigens.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Cetuximab, an anti-epidermal growth factor receptor (EGFR) antibody, has been shown to improve survival in nasopharyngeal carcinoma (NPC) patients. However, a correlation between the expression of EGFR and the response to cetuximab has not been observed, indicating that the mechanism underlying the effects of cetuximab needs to be further elucidated. The antitumour response involves immunotherapeutic mechanisms that target tumour-associated antigens, including complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC), act either alone or, more often, in combination. However, EBV infected NPC cells often develop resistance mechanisms that allow them to evade immune surveillance. Here, we found that overexpression of the complement-regulated protein CD55 in EBV-associated NPC cells mainly suppresses ADCC activity thus reduces the efficacy of cetuximab. Mechanistically, EBV latent membrane protein 1 (LMP1) mediated upregulation of CD55 through the NF-κB signalling pathway. The present study provides a rationale for the development of CD55 inhibitors to improve the clinical efficacy of cetuximab in NPC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.