系统性炎症标志物对egfr突变型非小细胞肺癌的影响。

IF 3.4 2区医学 Q2 ONCOLOGY

BMC Cancer Pub Date : 2025-10-04 DOI:10.1186/s12885-025-14915-1

Supagone Wangsubtawee, Thanaporn Thamrongjirapat, Narumol Trachu, Pimpin Incharoen, Natini Jinawath, Passaworn Cheyasawan, Nanamon Monnamo, Dittapol Munthum, Nattanan Reungwetwattana, Salin Amponnavarat, Pimtip Sanvarinda, Arthit Chairoungdua, Montien Ngodngamtaweesuk, Khantong Khiewngam, Ekaphop Sirachainan, Phichai Chansriwong, Thitiya Dejthevaporn, Thanyanan Reungwetwattana, Putthapoom Lumjiaktase

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引用次数: 0

摘要

背景：EGFRm肺癌在亚洲人群中有较高的患病率。临床前数据表明，PM2.5激活的炎症细胞因子影响EGFRm克隆扩增。在这里，我们探讨了炎症标志物与非小细胞肺癌EGFRm之间的相关性。方法：纳入2016-2023年切除的NSCLC患者。肿瘤组织和血清取自Ramathibodi肿瘤生物库。在同一患者的癌组织中采用rt-PCR检测EGFR 19del和L858R突变，在正常组织中采用dPCR检测EGFR 19del和L858R突变。采用ELISA法检测癌组织和正常组织中NF-Kb和STAT3蛋白信号的表达。流式细胞术检测血清中细胞因子（IL-1ß、IL-6、IL-8、IL-10、IL-12、TNF-α）的含量。结果：140例患者中，EGFRm在癌组织中的患病率为58%，在正常组织中的患病率仅为5%。NF-kB和STAT3在癌组织中高于正常组织[NF-kB中位od值=0.82 (IQR; 0.07-2.82) vs. 0.32 (IQR; 0.05-2.48)， P结论：炎症可能是NSCLC和EGFRm肺癌的发病机制之一，我们的前期研究证实了这一点。STAT3是一种潜在的炎症预测生物标志物。需要更大的队列。

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The impact of systemic inflammatory markers on EGFR-mutant non-small cell lung cancer.

Background: High prevalence of EGFRm lung cancer was found in the Asian population. Preclinical data suggest that inflammatory cytokines activated by PM2.5 affected EGFRm clone expansion. Here, we explored the correlation between inflammatory markers and EGFRm NSCLC.

Methods: Resected NSCLC patients (2016-2023) were enrolled. Tumor tissues and blood serum were retrieved from Ramathibodi tumor biobank. EGFR 19del and L858R mutations were performed by rt-PCR in cancerous tissue and dPCR in normal tissue in the same patient. NF-Kb and STAT3 protein signaling were measured by ELISA in both cancerous and normal tissue. Cytokines (IL-1ß, IL-6, IL-8, IL-10, IL-12 and TNF-α) were explored in serum by flow cytometry.

Results: Among 140 patients, EGFRm prevalence was 58% in cancerous tissue but only 5% in normal tissue. NF-kB and STAT3 were statistically higher in cancerous tissue than normal tissue [NF-kB median O.D.=0.82 (IQR; 0.07-2.82) vs. 0.32 (IQR; 0.05-2.48), P < 0.001; STAT3 median O.D.=0.32 (IQR; 0.10-1.58) vs. 0.17 (IQR; 0.06-1.29, P < 0.001]. STAT3 was significantly increased in EGFRm compared to EGFRwt [median O.D.=0.36 (IQR; 0.234-0.592) vs. 0.23 (IQR; 0.158-0.409), OR = 11.09 (95% CI; 2.17-56.58), P = 0.004]. TNF-α, IL-10, and STAT3 in cancer cells were higher in EGFRm than EGFRwt (P = 0.003, 0.008, and < 0.001, respectively). None of cytokines was statistically different between EGFRm and EGFRwt patients. However, only STAT3 in cancer cells and non-smoker were associated with EGFRm NSCLC in multivariable analysis.

Conclusion: Inflammation could be one of the pathogenesis of both NSCLC and EGFRm lung cancer as we demonstrated in our pilot study. STAT3 is a potentially inflammatory-predictive biomarkers. Larger cohort is needed.

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来源期刊

BMC Cancer 医学-肿瘤学

CiteScore

6.00

自引率

2.60%

发文量

1204

审稿时长

6.8 months

期刊介绍： BMC Cancer is an open access, peer-reviewed journal that considers articles on all aspects of cancer research, including the pathophysiology, prevention, diagnosis and treatment of cancers. The journal welcomes submissions concerning molecular and cellular biology, genetics, epidemiology, and clinical trials.