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急性髓系白血病（AML）患者诊断时骨髓穿刺液中髓系细胞胚胎抗原及其信号通路的高维质谱流式细胞术分析

High-Dimensional Mass Cytometry Analysis of Embryonic Antigens and Their Signaling Pathways in Myeloid Cells from Bone Marrow Aspirates in AML Patients at Diagnosis.

作者信息

Aanei Carmen-Mariana, Devêvre Estelle, Șerban Adrian, Tavernier-Tardy Emmanuelle, Guyotat Denis, Campos Catafal Lydia

机构信息

Laboratory of Hematology, University Hospital of Saint-Etienne, 42055 Saint-Etienne, France.

Santé Ingénierie Biologie Saint-Etienne, INSERM SainBiose U1059, 42270 Saint-Priest-en-Jarez, France.

出版信息

Cancers (Basel). 2023 Sep 25;15(19):4707. doi: 10.3390/cancers15194707.

DOI:10.3390/cancers15194707
PMID:37835401
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10571794/
Abstract

BACKGROUND

Embryonic antigens (EA) regulate pluripotency, self-renewal, and differentiation in embryonic stem (ES) cells during their development. In adult somatic cells, EA expression is normally inhibited; however, EAs can be re-expressed by cancer cells and are involved in the deregulation of different signaling pathways (SPs). In the context of AML, data concerning the expression of EAs are scarce and contradictory.

METHODS

We used mass cytometry to explore the expression of EAs and three SPs in myeloid cells from AML patients and normal bone marrow (NBM). Imaging flow cytometry was used for morphological assessment of cells in association with their OCT3/4 expression status (positive vs. negative).

RESULTS

An overall reduction in or absence of EA expression was observed in immature myeloid cells from AML patients compared to their normal counterparts. Stage-specific embryonic antigen-3 (SSEA-3) was consistently expressed at low levels in immature myeloid cells, whereas SSEA-1 was overexpressed in hematopoietic stem cells (HSCs) and myeloblasts from AML with monocytic differentiation (AML M4/M5). Therefore, these markers are valuable for distinguishing between normal and abnormal myeloid cells. These preliminary results show that the exploration of myeloid cell intracellular SPs in the setting of AML is very informative. Deregulation of three important leukemogenic SPs was also observed in myeloid cells from AML.

CONCLUSIONS

Exploring EAs and SPs in myeloid cells from AML patients by mass cytometry may help identify characteristic phenotypes and facilitate AML follow-up.

摘要

背景

胚胎抗原（EA）在胚胎干细胞发育过程中调节多能性、自我更新和分化。在成体细胞中，EA表达通常受到抑制；然而，癌细胞可重新表达EA，并参与不同信号通路（SP）的失调。在急性髓系白血病（AML）的背景下，关于EA表达的数据稀少且相互矛盾。

方法

我们使用质谱流式细胞术来探究AML患者和正常骨髓（NBM）髓系细胞中EA和三种SP的表达。成像流式细胞术用于结合细胞的八聚体转录因子3/4（OCT3/4）表达状态（阳性与阴性）对细胞进行形态学评估。

结果

与正常对照相比，AML患者未成熟髓系细胞中观察到EA表达总体降低或缺失。阶段特异性胚胎抗原-3（SSEA-3）在未成熟髓系细胞中始终低水平表达，而SSEA-1在具有单核细胞分化的AML（AML M4/M5）的造血干细胞（HSC）和成髓细胞中过表达。因此，这些标志物对于区分正常和异常髓系细胞很有价值。这些初步结果表明，在AML背景下探索髓系细胞内SP非常有意义。在AML的髓系细胞中也观察到三种重要的致白血病SP的失调。

结论

通过质谱流式细胞术探索AML患者髓系细胞中的EA和SP可能有助于识别特征性表型并促进AML的随访。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/b1fceba3f7b6/cancers-15-04707-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/2f202c1dbb7f/cancers-15-04707-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/e3f46c46b4f0/cancers-15-04707-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/9d88de3a4dc3/cancers-15-04707-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/b61c948ec7c7/cancers-15-04707-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/f4bc39571c1f/cancers-15-04707-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/a7d0a239c9ee/cancers-15-04707-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/b1fceba3f7b6/cancers-15-04707-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/2f202c1dbb7f/cancers-15-04707-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/e3f46c46b4f0/cancers-15-04707-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/9d88de3a4dc3/cancers-15-04707-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/b61c948ec7c7/cancers-15-04707-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/f4bc39571c1f/cancers-15-04707-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/a7d0a239c9ee/cancers-15-04707-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a78f/10571794/b1fceba3f7b6/cancers-15-04707-g007.jpg

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