骨髓脂肪细胞在 B 细胞急性淋巴细胞白血病中的动态演变:从诊断到化疗后的启示。

IF 4.4 4区 医学 Q2 ONCOLOGY Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-03-11 DOI:10.1080/15384047.2024.2323765
Xi Jia, Naying Liao, Yunqian Yao, Xutao Guo, Kai Chen, Pengcheng Shi
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引用次数: 0

摘要

脂肪细胞是骨髓微环境(BMM)中独特而多变的组成部分。然而,骨髓(BM)脂肪细胞从诊断为 B 细胞急性淋巴细胞白血病(B-ALL)到治疗后状态的动态演变,以及它们如何影响白血病的进展,仍未得到充分阐述。本研究采用了原代患者异种移植模型(PDX)和基质细胞共培养系统。我们发现,从 B-ALL 最初诊断到化疗后阶段,BM 脂肪细胞发生了动态演变,从最初白血病龛中的细胞耗竭过渡到缓解后的完全恢复状态。BM 脂肪细胞的增加会延缓 B-ALL 细胞在 PDX 模型中的移植,并抑制 B-ALL 细胞在体外的生长。从机理上讲,B-ALL 细胞在脂肪细胞富集的龛位中增殖受阻,可能是由于脂肪细胞本身分泌脂肪连素,而间充质干细胞(MSCs)不分泌细胞因子。总之,我们的发现为进一步深入了解BMM与B-ALL之间的动态平衡提供了一个新的视角。
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Dynamic evolution of bone marrow adipocyte in B cell acute lymphoblastic leukemia: insights from diagnosis to post-chemotherapy.

Adipocyte is a unique and versatile component of bone marrow microenvironment (BMM). However, the dynamic evolution of Bone Marrow (BM) adipocytes from the diagnosis of B cell Acute Lymphoblastic Leukemia (B-ALL) to the post-treatment state, and how they affect the progression of leukemia, remains inadequately explicated. Primary patient-derived xenograft models (PDXs) and stromal cell co-culture system are employed in this study. We show that the dynamic evolution of BM adipocytes from initial diagnosis of B-ALL to the post-chemotherapy phase, transitioning from cellular depletion in the initial leukemia niche to a fully restored state upon remission. Increased BM adipocytes retards engraftment of B-ALL cells in PDX models and inhibits cells growth of B-ALL in vitro. Mechanistically, the proliferation arrest of B-ALL cells in the context of adipocytes-enrichment niche, might attribute to the presence of adiponectin secreted by adipocytes themselves and the absence of cytokines secreted by mesenchymal stem cell (MSCs). In summary, our findings offer a novel perspective for further in-depth understanding of the dynamic balance between BMM and B-ALL.

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来源期刊
Cancer Biology & Therapy
Cancer Biology & Therapy 医学-肿瘤学
CiteScore
7.00
自引率
0.00%
发文量
60
审稿时长
2.3 months
期刊介绍: Cancer, the second leading cause of death, is a heterogenous group of over 100 diseases. Cancer is characterized by disordered and deregulated cellular and stromal proliferation accompanied by reduced cell death with the ability to survive under stresses of nutrient and growth factor deprivation, hypoxia, and loss of cell-to-cell contacts. At the molecular level, cancer is a genetic disease that develops due to the accumulation of mutations over time in somatic cells. The phenotype includes genomic instability and chromosomal aneuploidy that allows for acceleration of genetic change. Malignant transformation and tumor progression of any cell requires immortalization, loss of checkpoint control, deregulation of growth, and survival. A tremendous amount has been learned about the numerous cellular and molecular genetic changes and the host-tumor interactions that accompany tumor development and progression. It is the goal of the field of Molecular Oncology to use this knowledge to understand cancer pathogenesis and drug action, as well as to develop more effective diagnostic and therapeutic strategies for cancer. This includes preventative strategies as well as approaches to treat metastases. With the availability of the human genome sequence and genomic and proteomic approaches, a wealth of tools and resources are generating even more information. The challenge will be to make biological sense out of the information, to develop appropriate models and hypotheses and to translate information for the clinicians and the benefit of their patients. Cancer Biology & Therapy aims to publish original research on the molecular basis of cancer, including articles with translational relevance to diagnosis or therapy. We will include timely reviews covering the broad scope of the journal. The journal will also publish op-ed pieces and meeting reports of interest. The goal is to foster communication and rapid exchange of information through timely publication of important results using traditional as well as electronic formats. The journal and the outstanding Editorial Board will strive to maintain the highest standards for excellence in all activities to generate a valuable resource.
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