Immune checkpoint inhibitors (ICIs) are a recent breakthrough in antitumor drugs, although their overall safety has not been fully defined. Compared to conventional chemotherapy, ICIs exhibit different patterns of immunotoxicity, and immune-related adverse events (irAEs) have an immunological basis that is more toxic than usual and have a broad spectrum of manifestations involving different organ systems. Early recognition of symptoms and timely intervention are very important in managing immunerelated adverse events (irAEs). In this study, we report a case of delayed immune thrombocytopenia in a patient treated with nivolumab for small cell lung cancer (SCLC). We found that thrombocytopenia was associated with the presence of platelet antibodies, autoantibodies, and thyroglobulin antibodies, accompanied by a decrease in the number of helper T cells and regulatory T cells. Platelets returned to normal after the removal of antibodies by plasma exchanges and methylprednisolone. We hypothesized that thrombocytopenia in patients was an antibody-driven and T-cell-mediated process. Although these observations indirectly suggest that cytokine changes contribute to immune dysregulation during irAE, prospective validation is needed to explain the confounding etiologies that may contribute to cytokine dysregulation. Therefore, studying the relationship between T cell subpopulations, cytokines and irAE in a larger population may be crucial for identifying biomarkers for ICI.
Background: MicroRNA is involved in the development of lymphoma. It is reported that miR-361-3p has a tumor inhibitory effect, but its role in lymphoma is still unclear. The purpose of this study is to examine whether miR-361-3p can inhibit the development of lymphoma and further explore the related potential mechanism. Methods: In this study, we first analyzed the biological function of miR-361-3p in transfected Raji that mimicked miRNA. We also analyzed the biological function of the whole population in stably expressed miR-361-3p transgenic cells. Next, we conducted a complete micro-gene network to test the genetic profile of differential expression of stable gene-modified cells. Results: We found that miR-361-3p expression was often reduced in lymphoma cell lines. Cellular assays have shown a significant role in inhibiting the growth of miR-361-3p by inhibiting lymphoma proliferation and migration, and severely inhibiting the Wnt/β-catenin series protein signal. Bioinformatics analysis shows that Wnt10A is a new target of miR-361-3p, which is confirmed by our mechanism research. It is confirmed that restoring Wnt10A can reduce the tumor inhibition of Wnt/β-catenin during lymphoma progression and restore the normal signal of Wnt/β-catenin series proteins. Discussion: Our data indicate that miR-361-3p inhibits the Wnt/β-catenin protein signal by locking Wnt10A, which is an important factor in inhibiting the tumor in the pathogenesis of lymphoma. The miR-361-3p/Wnt10A axis may be a promising target for the treatment of lymphoma.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.