RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Il-6 and MSH3 in colorectal carcinoma: Expression, relationship, and prognostic significance in 171 colorectal carcinoma cases.
Il-6 and MSH3 in colorectal carcinoma: Expression, relationship, and prognostic significance in 171 colorectal carcinoma cases.
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本研究未显示 IL-6 与 MSH3 表达之间存在关联。由于 MSH3 是一种相对鲜为人知的蛋白,需要进一步开展大规模研究。未来使用 IHC 来识别可能从抗 IL-6 治疗中获益的 CRC 患者可能至关重要。
结直肠癌(CRC)是胃肠道最常见的癌症类型,其发生大多由环境因素导致。炎症在其病因中相对少见但却是重要的促成因素,而且炎症也被认为在没有临床诊断炎症性肠病的患者中构成风险。在细胞系中,促炎细胞因子白细胞介素-6(IL-6)导致错配修复蛋白MSH3发生胞质转移,并伴随功能丧失。本研究旨在通过免疫组织化学(IHC)评估171例散发性CRC样本中IL-6和MSH3的表达。假设高水平的IL-6会导致MSH3表达缺失。我们还探讨了IHC检测到的MSH3缺失的临床/病理学方面,以及MSH3表达与TIL(肿瘤浸润淋巴细胞)(TILs)之间的关系。
IL-6和MSH3 IHC以及H和E切片由两名病理学家评估。临床数据从该机构数据库中获取。
MSH3缺失与IL-6表达之间的关系未得到证实(P = 0.963)。在TILs高的患者组中,MSH3染色显著降低(P = 0.035)。我们观察到104例CRC病例(60.8%)存在IL-6表达,85例(49.7%)存在MSH3表达降低。
IL-6 and MSH3 IHC and H and E slides were evaluated by two pathologists. Clinical data were obtained from the institution's database.
A relationship between MSH3 loss and IL-6 expression was not proven ( P = 0.963). MSH3 staining was significantly reduced in the patient group with high TILs ( P = 0.035). We observed 104 CRC cases (60.8%) with IL-6 expression and 85 cases (49.7%) with reduced MSH3 expression.
This study did not demonstrate an association between IL-6 and MSH3 expression. As MSH3 is a relatively little-known protein, further large-scale studies are needed. The use of IHC to identify patients who may benefit from anti-IL-6 therapies in CRC in the future may be critical.
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