ArticleTheranostics2026
Globo H ceramide confers chemoresistance and poor prognosis to advanced gallbladder cancer via A2AR/cAMP/PKA pathway.
Article in Theranostics, 2026. 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.
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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.
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Who cites it
2 citing papers in PubMed.
- High Expression of SSEA3 and Globo H Predicts Poor Outcomes in Resected Extrahepatic Cholangiocarcinoma: A Single-Center Retrospective Cohort Study.Cancer medicine · 2026Article
- Adenosine signaling in tumor immune escape: metabolic checkpoints, myeloid suppression, and combination immunotherapy.Frontiers in oncology · 2026Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rationale: Gallbladder cancer (GBC) has poor prognosis, is primarily treated with gemcitabine-based chemotherapy, which is limited by gemcitabine correlates with GBC progression. This study investigate the role of Globo H ceramide (GHCer) in GR and explore whether targeting Glob H could overcome resistance Methods: Globo H expression was assessed by immunohistochemistry in 81 GBC samples. GHCer-induced GR and ABCG2 upregulation were assessed in GBC cell lines, patient-derived xenograft (PDX), and a thioacetamide (TAA)-induced rat cholangiocarcinoma model. A2AR/cAMP/PKA signaling involvement was examined using inhibitors and siRNA. The efficacy of anti-Globo H antibody (mAb VK9) or vaccine (OBI-833/OBI-821) combined with gemcitabine was evaluated Results: High Globo H expression correlated with shorter survival in GBC patients receiving gemcitabine. GHCer promoted GR via A2AR/cAMP/PKA-mediated ABCG2 upregulation, which was reversed by mAb VK9 or pathway inhibition. mAb VK9 or OBI-833/821 enhanced gemcitabine efficacy in GBC PDX and TAA cholangiocarcinoma models. OBI-833/821 induced anti-Globo H IgG/IgM, reduced Foxp3⁺ Tregs, and increased CD161⁺ NK cells in TAA model. A compassionate clinical use of 833/821 led to stable disease. Conclusions: GHCer promotes GR by upregulating ABCG2 via A2AR/cAMP/PKA signaling. Targeting Globo H may improve chemotherapy response in GBC.
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