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作为治疗耐药APL的GHRH对手的应用

Ravinder S Chale¹, Stephanie M Almeida¹, Mario Rodriguez¹

¹Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, Miller School of Medicine, University of Miami, 1600 NW 10th Ave RMSB R250, Miami, FL 33136, USA.

|June 28, 2023

概括

增长激素释放激素 (GHRH) 反对者MIA-602抑制了癌细胞的增殖. MIA-602在治疗各种癌症方面表现有前途,包括急性肌肉细胞白血病 (APL) 和急性肌肉细胞白血病 (AML).

科学领域:

在瘤学瘤学.
内分泌学在内分泌学.
分子生物学分子生物学

背景情况:

生长激素释放激素 (GHRH) 刺激恶性细胞的增殖.
像MIA-602这样的GHRH抗剂以前已经在抑制各种人类癌症细胞系方面表现出有效性.
在特定的白血病模型中,GHRH受体 (GHRH-R) 的存在和作用需要进一步阐明.

研究的目的:

调查NB4,NB4-RAA和K-562白血病细胞系中GHRH-R的存在.
评估GHGH抗体MIA-602在抑制这些细胞系的增殖中的疗效,在体外和体内.
评估MIA-602与急性髓性白血病 (AML) 的标准化疗相结合的协同效应.

主要方法:

在NB4,NB4-RAA和K-562细胞系中检测GHRH-R表达.
用MIA-602治疗的白血病细胞系的体外增殖试验.
在体内研究中,使用与MIA-602治疗的人类APL细胞系的异种移植.
结合疗法实验涉及MIA-602和多克索鲁比辛 (DOX) 在K-562AML细胞中.

主要成果:

在NB4,NB4-RAA和K-562细胞系中证实了GHRH-R的表达.
在实验室中,MIA-602显著抑制了所有三个测试的白血病细胞系的增殖.
用MIA-602治疗导致人类APL异种移植模型中的瘤生长大幅减少.
结合治疗MIA-602和多克索鲁比辛在减少K-562AML细胞增殖方面表现出协同效应.

结论:

MIA-602有效地抑制了GHRH-R表达白血病细胞系.
MIA-602证明了作为单一药物和AML的组合疗法的治疗潜力.
MIA-602可以克服对标准疗法的耐药性,如全转网红酸 (ATRA) 和三氧化 (ATO),并增强基于 antracycline 的疗法.

关键词:

在AML,AML就是AML.在APL中,APL是APL.在MIA-602中,它是MIA-602.增长激素释放激素的激素电阻的电阻是指电阻的电阻

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