ArticleClinical case reports2024
A Novel Intersection: Cytomegalovirus Gastritis Following Cemiplimab and Talimogene Laherparepvec in a Patient With Advanced Cutaneous Squamous Cell Carcinoma.
Article in Clinical case reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- A case of irAE gastritis caused by cemiplimab administration.Fujita medical journal · 2026Article
- Pre-treatment endocrine-nutritional signatures predict clinical benefit from PD-1/PD-L1 blockade in hematologic malignancies.Frontiers in nutrition · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytomegalovirus (CMV) reactivation is a rare complication in patients treated with immune checkpoint inhibitors (ICIs), typically occurring after immunosuppressive therapy for immune-related adverse events (irAEs). Here, we report a unique case of severe CMV gastritis in a patient receiving cemiplimab, an anti-PD-1 antibody, and talimogene laherparepvec (T-VEC), an oncolytic virus, without prior irAEs or immunosuppressive treatment. A 63-year-old man with advanced cutaneous squamous cell carcinoma received cemiplimab for one year and a single T-VEC injection for recurrent disease. He presented with progressive dyspepsia, significant weight loss, and malnutrition requiring total parenteral nutrition. Endoscopy revealed extensive gastric ulceration, and biopsies confirmed CMV gastritis. Initial treatment with intravenous ganciclovir improved his viral load but provided minimal symptomatic relief. After six weeks of therapy, biopsies showed resolution of CMV infection, and the patient transitioned to oral valganciclovir for prophylaxis while resuming cancer treatment. This case highlights the potential for CMV reactivation in patients undergoing ICI therapy, even without prior immunosuppression or irAEs. Notably, the concurrent use of T-VEC raises questions about the interplay between oncolytic viruses, ICIs, and immune modulation. Although T-VEC is not known to directly cause CMV reactivation, its role in amplifying immune responses warrants further investigation. As ICIs and oncolytic viruses become increasingly integral in oncology, clinicians must remain vigilant for rare infectious complications like CMV reactivation. Further research is needed to elucidate mechanisms, identify risk factors, and optimize management strategies for these events.
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Registered trials
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