结直肠癌中 KRAS 表达与 KRAS 状态、预后和肿瘤浸润 T 淋巴细胞的关系。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2024-05-15 eCollection Date: 2024-01-01 DOI:10.1177/17562848241249387
Yebohao Zhou, Ziwei Zeng, Ze Li, Lei Ruan, Hao Xie, Fujin Ye, Liang Huang, Huashan Liu, Liang Kang
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引用次数: 0

摘要

背景:克氏大鼠肉瘤病毒癌基因(KRAS)突变在结直肠癌(CRC)中的重要性已得到公认,但其与 KRAS 表达和预后之间的关系仍有待进一步研究。虽然 KRAS 的高表达通常与其他癌症的较差预后有关,但其在 CRC 中的作用仍未得到充分研究:探讨 KRAS 表达、KRAS 状态、预后和肿瘤浸润 T 淋巴细胞密度在 CRC 中的相关性:设计:单中心回顾性研究:本研究在2010年至2020年间进行,利用肿瘤样本评估KRAS表达并量化CD3+/CD8+ T淋巴细胞。采用Cox比例危险模型和线性回归分析来研究KRAS表达、预后和肿瘤浸润T淋巴细胞之间的关系:该研究纳入了265名接受根治性手术的CRC患者。KRAS表达与KRAS状态之间无明显关联(P>0.05)。KRAS 高表达与较差的总生存率和无病生存率相关(p p p > 0.05)。值得注意的是,KRAS 的表达与肿瘤组织中 CD8+ T 淋巴细胞的密度呈负相关(p p 结论:KRAS 的表达与肿瘤组织中 CD8+ T 淋巴细胞的密度无关:在 CRC 中未发现 KRAS 表达与 KRAS 突变状态之间存在关联。KRAS 表达越高,表明 CRC 患者的预后越差,错配修复能力强和 KRAS 野生型患者除外。此外,在 dMMR 患者中,KRAS 表达与肿瘤组织中 CD8+ T 淋巴细胞密度较低有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The relationship of KRAS expression with KRAS status, prognosis, and tumor-infiltrated T lymphocytes in colorectal cancer.

Background: The significance of Kirsten rat sarcoma viral oncogene (KRAS) mutation in colorectal cancer (CRC) is well established; yet, its association with KRAS expression and prognosis warrants further investigation. While high KRAS expression is commonly linked with poorer prognosis in other cancers, its role in CRC remains relatively understudied.

Objective: To explore the correlation between KRAS expression, KRAS status, prognosis, and tumor-infiltrating T lymphocyte density in CRC.

Design: Single-center retrospective study.

Methods: Conducted between 2010 and 2020, this study utilized tumor samples to assess KRAS expression and quantify CD3+/CD8+ T lymphocytes. The Cox proportional hazards model and linear regression analysis were employed to examine the relationship between KRAS expression, prognosis, and tumor-infiltrating T lymphocytes.

Results: This study included 265 CRC patients who underwent radical surgery. No significant association was observed between KRAS expression and KRAS status (p > 0.05). High KRAS expression was associated with poorer overall survival and disease-free survival (p < 0.05). Subgroup analysis revealed that high KRAS expression remained indicative of a worse prognosis in the group with mismatch repair-deficient (dMMR) and KRAS mutant type (p < 0.05). Multivariate analysis confirmed KRAS expression as an unfavorable prognostic factor (p < 0.05). However, the significance of KRAS expression was lost in the dMMR and KRAS mutant-type group regarding overall survival (p > 0.05). Notably, KRAS expression showed a negative correlation with the density of CD8+ T lymphocytes in tumor tissue (p < 0.05), a finding also observed in the dMMR group (p < 0.05).

Conclusion: No association was found between KRAS expression and KRAS mutation status in CRC. Higher KRAS expression was indicative of poorer prognosis for CRC patients, except for those with proficient mismatch repair and KRAS wild type. In addition, in patients with dMMR, KRAS expression was associated with a lower density of CD8+ T lymphocytes in tumor tissue.

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