IJLH:细胞凋亡可以作为儿童急性髓系白血病高风险表型的生物标志物?

2019-06-02 不详 网络

已经有研究在急性髓性白血病(AML)中探索了细胞凋亡的调节异常;然而,它与儿科AML临床结果的相关性尚不清楚。本研究旨在分析儿童AML患者通过内在途径介导的细胞凋亡和凋亡百分比以及临床结果。 本前瞻性研究纳入2013年7月至2016年8月登记的儿童AML患者。流式细胞仪检测基线骨髓(BM)中Annexin‐V(总凋亡标志物)和caspase‐9(内在通路标志物)的表达,并与对照组(未受实体瘤

已经有研究在急性髓性白血病AML)中探索了细胞凋亡的调节异常;然而,它与儿科AML临床结果的相关性尚不清楚。本研究旨在分析儿童AML患者通过内在途径介导的细胞凋亡和凋亡百分比以及临床结果。

本前瞻性研究纳入20137月至20168月登记的儿童AML患者。流式细胞仪检测基线骨髓(BM)AnnexinV(总凋亡标志物)caspase9(内在通路标志物)的表达,并与对照组(未受实体瘤影响的BM和未受影响的同胞外周血[PB]进行比较。使用logrank测试比较总体生存期(OS)和无事件生存期(EFS)

本研究共纳入151AML患者,中位年龄10(范围:0.718)AML患者中AnnexinV的表达明显高于实体瘤患者的BM (P = 0.01)和健康患者的PB (P = 0.04)Caspase9在胚细胞中的表达无显著差异。在WBC计数≥11000 /mm3 (P = 0.02)、‐细胞遗传学不良(P = 0.02)RUNX1RUNX1T1易位缺失(P = 0.004)NPM1突变缺失(P = 0.05)的患者中,annexinV的中位表达显著增高。高annexinV表达的患者在单因素分析中OS明显低于对照组(P = 0.05),而在多因素分析中则无差异(P = 0.32)

研究表明,急性髓系白血病(AML)基线BM标本中细胞凋亡总体呈激活状态。在该疾病中,高凋亡可能与高风险表型有关。

原始出处:

Anudishi Tyagi, Raja Pramanik,Apoptosis: A biomarker of highrisk phenotype in pediatric acute myeloid leukemia?

本文系梅斯医学(MedSci)原创编译整理,转载需授权!

 

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    2019-06-04 tastas
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Cell Death & Disease:c-FLIP和CD95对肾细胞癌的生存是必需的

透明细胞肾细胞癌(ccRCC)是肾脏癌症中最突出的肿瘤。肾细胞癌(RCC)岁肿瘤治疗的抗性可以归结于抗凋亡蛋白的过表达而引起的细胞凋亡的抗性等。然而,在ccRCC中,关于细胞凋亡抑制因子c-FLIP的作用和它对死亡受体诱导的细胞凋亡的影响所知甚少。最近,有研究人员阐释了c-FLIP在4个ccRCC细胞系中对CD95L诱导的细胞凋亡抗性的产生非常关键。明显的是,shRNA对c-FLIP表达的下调作用

INT J LAB HEMATOL:细胞凋亡是儿童急性髓系白血病高危表型生物标志物?

目前已经发现在急性髓系白血病(AML)中已会出现细胞凋亡的失调。然而,其与儿童AML临床结果的相关性尚不清楚。本研究旨在分析儿童AML患者的凋亡百分率及通过内在通路介导的凋亡与临床结局。 本前瞻性研究纳入2013年7月~ 2016年8月儿科AML患者。流式细胞术检测基线骨髓(BM)标本中Annexin V(总凋亡标志物)和caspase 9表达(固有通路标志物),并与对照组(实体瘤未受影响的

J Leukoc Biol:过敏性鼻炎患者中,白介素-5能够诱导CD4+T细胞凋亡缺陷

辅助性T细胞(Th)2极化在过敏性疾病的病理中具有重要的角色,而潜在的机制仍旧需要进一步的调查。类B细胞淋巴瘤蛋白-2蛋白12(Bcl2L12)具有抗凋亡的功能。最近,有研究人员阐释了过敏性鼻炎(AR)患者中,Bcl2L12对Th2极化的影响。研究发现,AR CD4+ T细胞(来源于AR患者)展现出了细胞凋亡的缺陷。FasL在AR CD4+ T细胞中表达要比HC(健康对照) CD4+ T细胞中更低

Blood:HAP1基因缺失可通过下调calpain-1-Bid-caspase-3/12信号通路使ALL患者对左旋 -天冬酰胺酶产生耐药性

中心点:ALL患者HAP1缺失可阻止L-ASNase诱发的ER Ca2+释放,抑制外源性Ca2+内流,减少Ca2+电位([Ca2+]i)升高和凋亡细胞。HAP1是一种ALL患者的新的L-ASNase耐药的生物标志物,可用于鉴别高危患者和设计L-ASNase耐药患者的治疗方案。摘要:左旋-天冬酰胺酶是急性淋巴细胞白血病(ALL)治疗方案的重要组成部分。它可导致天冬酰胺缺乏症,导致蛋白质合成抑制和白血