独立于KRAS和GNAS突变的A2AR表达和免疫抑制环境在Pseudomyxoma Peritonei中

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Shigeki Kusamura¹, Adele Busico², Elena Conca²

¹Peritoneal Surface Malignancy Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Venezian 1, 20133 Milan, Italy.

|July 29, 2023

概括

状瘤 (Pseudomyxoma peritonei,简称PMP) 呈现出像GM-CSF和A2AR这样的免疫抑制因子,与KRAS/GNAS突变无关. 在PMP瘤细胞中CD163表达表明预后不佳,这表明新的治疗和预后标.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

皮瘤 (Pseudomyxoma peritonei,简称PMP) 是一种罕见的恶性瘤,经常出现KRAS和GNAS突变.
这些突变被假设通过GM-CSF和A2AR信号抑制抗瘤免疫力.
在分子水平上,PMP的特征很差,因此需要探索免疫逃避机制.

研究的目的:

研究KRAS和GNAS突变促进PMP免疫监测逃逸的机制.
在PMP中识别潜在的治疗和预后目标.
为了将分子状态与免疫细胞透和临床结果相关联.

主要方法:

免疫组织化学用于评估40名PMP患者的GM-CSF,A2AR,CD73,CD39和PD-L1的表达.
免疫细胞群 (CD4 +,CD8 +,CD20 +,CD163 +,CD56 +) 通过免疫组织化学和NanoString nCounter®进行了分析.
患者被分为低风险和高风险组,基于PMP预后名录.

主要成果:

GM-CSF (74%),A2AR (74%),CD73 (53%),CD39 (37%) 和PD-L1 (16%) 都被表达出来,这些表达方式与KRAS/GNAS状态无关.
瘤微环境包括CD4+ T细胞 (86%),CD20+ B细胞 (67%),CD15+细胞 (86%),CD163+ M2巨细胞 (67%);NK细胞没有出现.
在PMP瘤细胞中CD163表达 (27%) 与预后不佳相关;高风险患者的无进展生存率和特定基因 (MET,IL8等) 的下调更差. ) 的情况.

结论:

免疫抑制因子GM-CSF,A2AR和PD-L1存在于PMP中,提供潜在的治疗点.
这些因素与KRAS或GNAS突变状态没有直接联系.
瘤细胞中的CD163表达和21个预后基因的小组需要进一步研究作为PMP的生物标志物.

关键词:

A2AR A2AR A2AR A2AR A2AR A2AR A2 CD39 CD39 是一个 CD73 CD73 CD73 CD73 CD73 CD73 CD73 CD73 CD73 CD73 CD73 CD73 在 PDL-1 中使用.伪性瘤 (pseudomyxoma peritonei) 是一种发生在人体内的疾病.

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