ArticlePloS one2013
Engagement of SIRPα inhibits growth and induces programmed cell death in acute myeloid leukemia cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- The characteristics of circRNA as competing endogenous RNA in pathogenesis of acute myeloid leukemia.BMC cancer · 2021Article
- Therapeutic modulation of the CD47-SIRPα axis in the pediatric tumor microenvironment: working up an appetite.Cancer drug resistance (Alhambra, Calif.) · 2020Review
- SIRPα expression delineates subsets of intratumoral monocyte/macrophages with different functional and prognostic impact in follicular lymphoma.Blood cancer journal · 2019Article
- Detection of Signal Regulatory Protein α inFrontiers in immunology · 2017Article
- "Stealth dissemination" of macrophage-tumor cell fusions cultured from blood of patients with pancreatic ductal adenocarcinoma.PloS one · 2017Article
- CD47 in the tumor microenvironment limits cooperation between antitumor T-cell immunity and radiotherapy.Cancer research · 2014Article
- Identification and targeting leukemia stem cells: The path to the cure for acute myeloid leukemia.World journal of stem cells · 2014Review
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Authors and funding
21 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent studies show the importance of interactions between CD47 expressed on acute myeloid leukemia (AML) cells and the inhibitory immunoreceptor, signal regulatory protein-alpha (SIRPα) on macrophages. Although AML cells express SIRPα, its function has not been investigated in these cells. In this study we aimed to determine the role of the SIRPα in acute myeloid leukemia. DESIGN AND
methodsWe analyzed the expression of SIRPα, both on mRNA and protein level in AML patients and we further investigated whether the expression of SIRPα on two low SIRPα expressing AML cell lines could be upregulated upon differentiation of the cells. We determined the effect of chimeric SIRPα expression on tumor cell growth and programmed cell death by its triggering with an agonistic antibody in these cells. Moreover, we examined the efficacy of agonistic antibody in combination with established antileukemic drugs.
resultsBy microarray analysis of an extensive cohort of primary AML samples, we demonstrated that SIRPα is differentially expressed in AML subgroups and its expression level is dependent on differentiation stage, with high levels in FAB M4/M5 AML and low levels in FAB M0-M3. Interestingly, AML patients with high SIRPα expression had a poor prognosis. Our results also showed that SIRPα is upregulated upon differentiation of NB4 and Kasumi cells. In addition, triggering of SIRPα with an agonistic antibody in the cells stably expressing chimeric SIRPα, led to inhibition of growth and induction of programmed cell death. Finally, the SIRPα-derived signaling synergized with the activity of established antileukemic drugs.
conclusionsOur data indicate that triggering of SIRPα has antileukemic effect and may function as a potential therapeutic target in AML.
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