ArticleCancer gene therapy2026
CD73 inhibitor enhances the antitumor activity of selinexor in multiple myeloma by restoring the activation of CD8
Article in Cancer gene therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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15 authors.
Funding
Abstract
Selinexor, a selective nuclear export inhibitor, blocks exportin-1 and reduces oncoprotein messenger RNA translation, and is approved for the treatment of relapsed/refractory multiple myeloma in combination with proteasome inhibitors, immunomodulators, anti-CD38 antibodies, etc. Nevertheless, selinexor presents limited monotherapy efficacy with an objective response rate of 29% and fails to completely overcome drug resistance. To improve the therapeutic outcome, this study investigated the combined treatment of selinexor and a CD73 inhibitor in a murine tumor model. The expression of CD73 in multiple tumor cell lines following selinexor treatment was first analyzed. In vivo experiments were performed on J558-inoculated BALB/c mice, which were divided into vehicle group, ATG-037 (CD73 inhibitor) monotherapy group, ATG-010 (selinexor) monotherapy group, and combination therapy group. Single-cell RNA sequencing (scRNA-seq) was utilized to characterize immune cell subtypes and tumor-immune crosstalk, and immunofluorescence staining was conducted on histological tumor samples. In addition, a co-culture model of CD8
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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 Socratic graph.