期刊
SURGERY TODAY
卷 51, 期 10, 页码 1671-1681出版社
SPRINGER
DOI: 10.1007/s00595-021-02273-x
关键词
Cancer niches; CCL2; Macrophage; Plasma tumor marker; Recurrence
类别
资金
- Japan Society for the Promotion of Science [JP16K07177, JP16K10543, JP16K19197, JP17K16454, JP17K16521, JP17K10593, JP17K19608]
- OITA Cancer Research Foundation
- Daiwa Securities Health Foundation
- Priority Issue on Post-K Computer [hp170227, hp160219]
- JSPS KAKENHI [15H05707]
- Eli Lilly Japan K.K. Grant
- Japanese Foundation for Multidisciplinary Treatment of Cancer
- [15H0912]
Plasma CCL2 is identified as a predictive biomarker for postoperative CRC recurrence, and is associated with the immune response of tumors.
Purpose There is currently no adequate biomarker for predicting colorectal cancer (CRC) recurrence. Chemokine (C-C motif) ligand 2 (CCL2) induces macrophages and fibroblasts to occupy metastatic niches in distant organs. The purpose of this study was to examine CCL2 as a potential predictive biomarker for CRC recurrence. Methods Plasma samples (n = 402) were collected from 80 stage II/III/IV CRC cases and the relationship between CCL2 profiles and recurrence was investigated. The tumor immune response genes associated with CCL2 mRNA expression in a subgroup of 8 stage I/II CRC cases with 12 recurrent sites and The Cancer Genome Atlas database were also analyzed retrospectively. Results Sixteen stage II/III/IV postoperative recurrent CRC cases experienced a significant increase in plasma CCL2 levels 6 months after surgery and continuously increased even after R0-1 resection. The 6-month postoperative CCL2 levels in recurrent cases of >= 1 year were significantly higher than in non-recurrent cases and recurrent cases of < 1 year. The CCL2 level in the primary tumor cases significantly correlated with the cytolytic activity, thus indicating a tumor immune response from the CD163-expressing macrophages. Conclusion Plasma CCL2 was found to be a predictive biomarker of postoperative CRC recurrence. CCL2 in metastatic sites derives from metastatic niches that surpass the host immune response.
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