ArticleCell death & disease2018
Midostaurin potentiates rituximab antitumor activity in Burkitt's lymphoma by inducing apoptosis.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
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- Putative role of natural products as Protein Kinase C modulator in different disease conditions.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2021Review
- Herbal NF-κB Inhibitors Sensitize Rituximab-Resistant B Lymphoma Cells to Complement-Mediated Cytolysis.Frontiers in oncology · 2021Article
- Xenograft models for pediatric cancer therapies.Faculty reviews · 2021Review
- [Menthol enhances interleukin-13-induced synthesis and secretion of mucin 5AC in human bronchial epithelial cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- The multiple-kinase inhibitor lenvatinib inhibits the proliferation of acute myeloid leukemia cells.Animal models and experimental medicine · 2019Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An intensive short-term chemotherapy regimen has substantially prolonged the overall survival of Burkitt's lymphoma (BL) patients, which has been further improved by addition of rituximab. However, the inevitable development of resistance to rituximab and the toxicity of chemotherapy remain obstacles. We first prepared two BL cell lines resistant to rituximab-mediated CDC. Using a phosphorylation antibody microarray, we revealed that PI3K/AKT pathway contained the most phosphorylated proteins/hits, while apoptosis pathway that may be regulated by PKC displayed the greatest fold enrichment in the resistant cells. The PI3K/AKT inhibitor IPI-145 failed to reverse the resistance. In contrast, the pan-PKC inhibitor midostaurin exhibited potent antitumor activity in both original and resistant cells, alone or in combination with rituximab. Notably, midostaurin promoted apoptosis by reducing the phosphorylation of PKC and consequently of downstream Bad, Bcl-2 and NF-κB. Therefore, midostaurin improved rituximab activity by supplementing pro-apoptotic effects. In vivo, midostaurin alone powerfully prolonged the survival of mice bearing the resistant BL cells compared to rituximab alone treatments. Addition of midostaurin to rituximab led to dramatically improved survival compared to rituximab but not midostaurin monotherapy. Our findings call for further evaluation of midostaurin alone or in combination with rituximab in treating resistant BL in particular.
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Registered trials
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