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在儿科B细胞前急性淋巴细胞白血病中,化学抵抗的分子和细胞机制
Caleb B Lill1,2, Stephen Fitter1,2, Andrew C W Zannettino1,2
1Myeloma Research Laboratory, School of Biomedicine, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, Australia.
Cancer metastasis reviews
|August 5, 2024
概括
复发的B细胞急性淋巴细胞白血病 (B-ALL) 是由于化学抵抗而具有挑战性的. 骨髓微环境细胞,如介质干细胞和脂肪细胞,支持B-ALL生存和治疗耐药性.
科学领域:
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
- 血液学 血液学 血液学
背景情况:
- 在儿童患者中复发的B细胞急性淋巴细胞白血病 (B-ALL) 预后不佳.
- 在复发性B-ALL中,化学阻力是一个重大的临床挑战.
- 骨髓微环境 (BMM) 在调节B-ALL化疗敏感性方面发挥着至关重要的作用.
研究的目的:
- 审查骨髓介质干细胞 (BM-MSCs) 和骨髓脂肪细胞对B-ALL化学抵抗有所贡献的分子机制.
- 探索针对这些BMM介导的抵抗机制的新型治疗策略.
主要方法:
- 文献综述侧重于B-ALL与BM-MSC和脂肪细胞的相互作用.
- 信号通路的分析,包括综合素介导信号和阿斯巴拉金补充剂.
- 检查脂肪细胞在药物隔离和利基形成中的作用.
主要成果:
- BM-MSCs通过整合素信号和氨酸供应支持B-ALL,增强化疗抵抗力.
- 脂肪细胞隔离人环素并创建一个支持的利基,促进B-ALL的生存.
- 无论是BM-MSC还是脂肪细胞都会导致静止的,耐化学反应的B-ALL表型.
结论:
- 针对B-ALL及其骨髓微环境之间的相互作用对于克服化学抵抗至关重要.
- 需要针对BM-MSC和脂肪细胞介导支持机制的新疗法,以改善复发性/耐药性B-ALL的结果.
- 了解这些依赖于利基的抵抗机制为治疗干预提供了新的途径.
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