Blood：IGF1R调节肿瘤对PI3K-δ抑制剂的耐药性

2019-04-23 秦启云 MedSci原创

靶向疗法正在彻底改变癌症的治疗，但耐药性极大阻碍了靶向疗法的发展与应用。PI3K-δ抑制剂Idelalisib已被批准用于治疗慢性淋巴细胞白血病（CLL）和非霍奇金淋巴瘤（NHL），但部分患者对其耐药的机制尚不明确。Annika Scheffold等人在小鼠中通过多次肿瘤移植和治疗在体内模拟PI3K-δ抑制剂耐药性的产生。并采用全外显子测序鉴定有无可解释对PI3K-δ抑制剂耐药的频发突变。在小鼠模

靶向疗法正在彻底改变癌症的治疗，但耐药性极大阻碍了靶向疗法的发展与应用。PI3K-δ抑制剂Idelalisib已被批准用于治疗慢性淋巴细胞白血病（CLL）和非霍奇金淋巴瘤（NHL），但部分患者对其耐药的机制尚不明确。

Annika Scheffold等人在小鼠中通过多次肿瘤移植和治疗在体内模拟PI3K-δ抑制剂耐药性的产生。并采用全外显子测序鉴定有无可解释对PI3K-δ抑制剂耐药的频发突变。

在小鼠模型中，PI3K-δ抑制剂耐药性的产生是由于耐药肿瘤中的胰岛素样生长因子1受体（IFG1R）激活，进而导致了MAPK信号增强。经体外过表达IFG1R，证实了其参与PI3K-δ抑制剂的耐药性。在对PI3K-δ抑制剂耐药的肿瘤中，IFG1R表达上调受FOXO1转录因子和糖原合成酶激酶3β（GSK3B）的功能性激活和核定位增强所调控。

在人类CLL中，高IGF1R表达与12号染色体三体相关。来源于Idelalisib治疗过的患者的CLL细胞，在体外对Idelalisib的敏感性降低；而且经Idelalisib暴露后，MAPK信号增强、IGF1R表达明显上调。

总而言之，本研究表明替代信号级联反应在癌细胞对PI3K-δ抑制剂耐药性产生过程中发挥重要作用，上述信号通路变化或可作为治疗靶点，抑制IGF1R或可作为PI3K-δ抑制剂耐药性肿瘤的补救疗法。

原始出处：

Annika Scheffold，et al.IGF1R as druggable target mediating PI3K-δ inhibitor resistance in a murine model of chronic lymphocytic leukemia. Blood 2019 ：blood.2018881029； doi： https：//doi.org/10.1182/blood.2018881029

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2020-03-17 839640778

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2019-06-18 jklm09

#抑制剂#

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2020-02-07 智者为医08

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2019-06-03 仁医06

#IGF#

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2019-04-25 ms1292405679162969

#PI3K#

30 0
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2020-01-31 12498cb5m22暂无昵称

#IGF1#

36 0

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