Expression and role of granulocyte macrophage colony-stimulating factor receptor (GM-CSFR) and granulocyte colony-stimulating factor receptor (G-CSFR) on Ph-positive acute B lymphoblastic leukemia

Wu, Yong; Tan, Ming; Chen, Mei‐Ling; Chen, Yuanzhong

doi:10.1080/10245332.2018.1426540

Cited by 3 publications

(2 citation statements)

References 25 publications

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“…Cell cycle, cell apoptosis, and cell surface antigens were detected using flow cytometry. In brief, 48 h after treatment of KG-1, Kasumi-1, KG-1a, TF-1, or primary cells, the cell density was adjusted according to the cell viability assay and prepared for cell cycle analysis as described in our previous report [17]. Cells were stained with Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) (BD Pharmingen, San Diego, CA, USA) to detect the apoptosis state in accordance with the manufacturer specifications.…”

Section: Methodsmentioning

confidence: 99%

Synergistic killing effects of homoharringtonine and arsenic trioxide on acute myeloid leukemia stem cells and the underlying mechanisms

Tan

Zhang

Yuan

et al. 2019

J Exp Clin Cancer Res

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Background At present, it is generally believed that leukemia stem cells are the source of AML, so the killing of leukemia stem cells has become important. Previous studies have suggested that HHT combined with ATO can synergistically kill U937 cells, and HHT has also demonstrated the ability to kill leukemia stem cells. We evaluated whether HHT combined with ATO can systematically kill leukemia stem cells (LSCs) and explored the synergistic effect and molecular mechanism. Methods CCK-8 was used to detect cell viability. The changes of cell cycle (PI staining), apoptosis (Annexin V/PI) and surface markers (CD34, CD38, CD96, CD45) were detected by flow cytometry. The cells of CD34+ primary leukemia and CD38- KG-1, and TF-1 were separated by flow cytometry. High-throughput mRNA sequencing was used to analysis mRNA level changes after the application of the two drugs. Western blot was used to verify the changes of pathway protein expression. NRG mice were used as the receptor of xenograft model. Histological H&E staining assess the invaded ability of leukemia cells, and laser scanning confocal microscopy evaluated the molecule markers change. Results HHT and ATO synergistically killed KG-1 (CD34 + /CD96 + /CD38 + / − ) and Kasumi-1 (CD34 + /CD38 − ) cells. Their combination had a stronger effect of inducing apoptosis and blocking the cell cycle than HHT or ATO administrator alone, meanwhile significantly reducing the numbers of LSCs. Further, CD34 + CD38 − cells in KG-1, KG-1a, TF-1, and primary leukemia cells were more sensitive to HHT and ATO. High-throughput mRNA sequencing suggested that HHT alone could significantly upregulate molecules related to the Notch, P53, and NF-κB signaling pathways. When combined with ATO, HHT further upregulated P53, whereas HHT-induced NF-κB pathway activation was significantly suppressed. Western blot analysis verified the change of protein expression in the above pathways and further demonstrated that GSI, could eliminate these effects. In vivo, HHT combined with ATO significantly reduced the LSC burden, and weakened the expression of LSC markers. Conclusions This is the first evidence that HHT combined with arsenic can synergistically kill LSCs in vitro and in vivo, along with identification of the underlying mechanism, highlighting a potentially effective treatment strategy. Electronic supplementary material The online version of this article (10.1186/s13046-019-1295-8) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

Synergistic killing effects of homoharringtonine and arsenic trioxide on acute myeloid leukemia stem cells and the underlying mechanisms

Tan

Zhang

Yuan

et al. 2019

J Exp Clin Cancer Res

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“…Although these mutations alone cannot cause a myeloproliferative neoplasms-phenotype and are frequently found in other hematologic malignancies, they seem to generally increase the genetic instability of the affected cells, thereby potentially giving them additional pro-oncogenic advantages and are probably able to modify disease progression. Wu et al 30 demonstrated high expression levels of GM-CSFR and G-CSFR, as well as their promotable role for viability in Ph+ ALL cells. They further found that recombinant human G-CSF (rhG-CSF) influenced the sensitivity of SUP-B15 (a Ph+ ALL cell line) cells to TKIs.…”

Section: Discussionmentioning

confidence: 99%

Colony-stimulating factor 3 receptor (CSF3R) M696T mutation does not impact on clinical outcomes of a Ph+ acute lymphoblastic leukemia patient

et al. 2021

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Colony-stimulating factor 3 receptor (CSF3R) mutations have been identified in a variety of myeloid disorders. Although CSF3R point mutations (eg, T618I) are emerging as key players in chronic neutrophilic leukemia/atypical chronic myelogenous leukemia , the significance of rarer CSF3R mutations is unknown. Here, we report a 32-year-old female who was diagnosed as Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph + ALL) with the CSF3R M696T mutation and was undergone unrelated donor hematopoietic stem cell transplantation. The patient achieved complete remission with chemotherapy in combination with tyrosine kinase inhibitor (TKI) and long-term survival by unrelated donor transplantation. Meanwhile, we performed a series of experiments using murine interleukin 3 (IL-3)-dependent Ba/F3 cell line to evaluate the transforming capacity of the CSF3R M696T mutation. We confirmed the presence of a CSF3R M696T germline mutation in this patient which was inherited from her mother. The in vitro experiment results showed that the CSF3R M696T mutation contributes marginally to the tumor transformation of Ba/F3 cells, indicating that CSF3R M696T mutation was neutral in tumor transformation ability. We concluded that TKI is effective in patients with the CSF3R M696T mutation in Ph + ALL and donors with CSF3R M696T mutation might still be selected as the candidate for transplantation.

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Evidence for adverse effects by G-CSF in some acute lymphoblastic leukemias

Kelley¹,

Cooling

2023

Transfusion and Apheresis Science

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Expression and role of granulocyte macrophage colony-stimulating factor receptor (GM-CSFR) and granulocyte colony-stimulating factor receptor (G-CSFR) on Ph-positive acute B lymphoblastic leukemia

Abstract: We demonstrated high expression levels of GM-CSFR and G-CSFR, as well as their promotable role for viability in ph + ALL cells. We further found that rhG-CSF influenced the sensitivity of SUP-B15 cells to TKIs.

Cited by 3 publications

References 25 publications

Synergistic killing effects of homoharringtonine and arsenic trioxide on acute myeloid leukemia stem cells and the underlying mechanisms

Synergistic killing effects of homoharringtonine and arsenic trioxide on acute myeloid leukemia stem cells and the underlying mechanisms

Colony-stimulating factor 3 receptor (CSF3R) M696T mutation does not impact on clinical outcomes of a Ph+ acute lymphoblastic leukemia patient

Evidence for adverse effects by G-CSF in some acute lymphoblastic leukemias

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