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在Xanthogranulomatous上皮瘤/素阳性巨细胞丰富瘤中CSF1的表达

Carina A Dehner¹, Ying-Chun Lo², Shefali Chopra³

¹Department of Anatomic Pathology and Laboratory Medicine, Indiana University, 635 Barnhill Drive, Indianapolis, IN, 46202, USA; Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 1st St SW, Rochester, MN, 55905, USA; Department of Pathology and Immunology, Division of Anatomic and Molecular Pathology, Washington University School of Medicine, 660 S. Euclid Ave, St. Louis, MO, 63110, USA.

Human pathology

|November 22, 2023

概括

桑托格兰瘤性上皮瘤 (XGET) 和素阳性巨细胞丰富软组织瘤 (KPGCT) 显示CSF1过度表达,这表明这种途径是它们发展的关键. 这一发现支持CSF1R抑制作为这些罕见瘤的潜在治疗方法.

科学领域:

在瘤学瘤学.
病理学病理学病理学
分子生物学分子生物学

背景情况:

桑托格兰瘤性上皮瘤 (XGET) 和素阳性巨细胞丰富软组织瘤 (KPGCT) 是最近发现的介质细胞瘤.
这些瘤在丰富的非新生性炎症细胞和囊细胞中具有少量瘤细胞,类似于瘤巨细胞瘤.
有证据表明,CSF1可能是XGET/KPGCT中特有的"景观效应"的帕克林因子.

研究的目的:

调查CSF1/CSF1R途径在XGET/KPGCT.病变发生过程中的作用.
为了测试CSF1在XGET/KPGCT中过度表达的假设.

主要方法:

使用定量实时PCR (qPCR) 来测量CSF1基因表达.
进行了CSF1 RNAscope染色在位杂交 (CISH),以评估CSF1的局部化和表达.
这项研究分析了6例XGET/KPGCT.

主要成果:

通过CISH,所有分析的XGET/KPGCT病例均为CSF1阳性.
在所有病例中,qPCR分析显示CSF1表达增加.
这些发现证实了XGET/KPGCT中CSF1过度表达.

结论:

这项研究提供了强有力的证据,表明CSF1/CSF1R途径参与了XGET/KPGCT的致病性.
这些结果表明,CSF1R抑制剂可能是不可切除或转移XGET/KPGCT的潜在治疗策略.

关键词:

在CSF1中,CSF1在CSF1中.巨细胞瘤是一个巨细胞瘤.在HMGA2:NCOR2中使用.氨酸阳性巨细胞丰富的瘤 RNA范围 CISH 的范围在Xanthogranulomatous上皮瘤.

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