scholarly journals M2 macrophage infiltration into tumor islets leads to poor prognosis in non-small-cell lung cancer

2019 ◽  
Vol Volume 11 ◽  
pp. 6125-6138 ◽  
Author(s):  
Lili Cao ◽  
Xiaofang Che ◽  
Xueshan Qiu ◽  
Zhi Li ◽  
Bowen Yang ◽  
...  
2018 ◽  
Vol 64 (4) ◽  
pp. 522-527
Author(s):  
Aleksey Shutko ◽  
Viktor Mus

Individual parameters of circulating hemopoietic stem cells (HSC) lymphoid origin were measured by cytofluorometry before treatment of patients with metastatic non-small cell lung cancer and were retrospectively compared with individual life span's (LS). The possibility of poor prognosis of treatment's results (LS


Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 3426-3433
Author(s):  
Juanjuan Yong ◽  
Liyun Huang ◽  
Gengbiao Chen ◽  
Xiaoya Luo ◽  
Hui Chen ◽  
...  

Biology ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 502
Author(s):  
David Dora ◽  
Christopher Rivard ◽  
Hui Yu ◽  
Shivaun Lueke Pickard ◽  
Viktoria Laszlo ◽  
...  

This study aims to characterize tumor-infiltrating macrophages (TAMs), myeloid-derived suppressor cells (MDSC), and the related molecular milieu regulating anti-tumor immunity in limited-stage neuroendocrine (NE)-high and NE-low small cell lung cancer. Primary tumors and matched lymph node (LN) metastases of 32 resected, early-stage SCLC patients were analyzed by immunohistochemistry (IHC) with antibodies against pan-macrophage marker CD68, M2-macrophage marker CD163, and MDSC marker CD33. Area-adjusted cell counting on TMAs showed that TAMs are the most abundant cell type in the TME, and their number in tumor nests exceeds the number of CD3 + T-cells (64% vs. 38% in NE-low and 71% vs. 18% in NE-high). Furthermore, the ratio of CD163-expressing M2-polarized TAMs in tumor nests was significantly higher in NE-low vs. NE-high tumors (70% vs. 31%). TAM density shows a strong positive correlation with CD45 and CD3 in tumor nests, but not in the stroma. fGSEA analysis on a targeted RNAseq oncological panel of 2560 genes showed that NE-high tumors exhibited increased enrichment in pathways related to cell proliferation, whereas in NE-low tumors, immune response pathways were significantly upregulated. Interestingly, we identified a subset of NE-high tumors representing an immune-oasis phenotype, but with a different gene expression profile compared to NE-low tumors. In contrast, we found that a limited subgroup of NE-low tumors is immune-deserted and express distinct cellular pathways from NE-high tumors. Furthermore, we identified potential molecular targets based on our expression data in NE-low and immune-oasis tumor subsets, including CD70, ANXA1, ITGB6, TP63, IFI27, YBX3 and CXCR2.


2017 ◽  
Vol 14 (4) ◽  
pp. 3959-3966 ◽  
Author(s):  
Dan Liu ◽  
Yi Huang ◽  
Li Zhang ◽  
Dong-Ni Liang ◽  
Li Li

2018 ◽  
Vol 45 (6) ◽  
pp. 2213-2224 ◽  
Author(s):  
Meng Zhao ◽  
Yahui Liu ◽  
Ran Liu ◽  
Jin Qi ◽  
Yongwang Hou ◽  
...  

Background/Aims: Cytokines are key players in tumorigenesis and are potential targets in cancer treatment. Although IL-6 has attracted considerable attention, interleukin 11 (IL-11), another member of the IL-6 family, has long been overlooked, and little is known regarding its specific function in non-small cell lung cancer (NSCLC). In this study, we explored IL-11’s role in NSCLC and the detailed mechanism behind it. Methods: Cell proliferation in response to IL-11 was determined by colony formation, BrdU incorporation and MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assay. Cell motility was measured by Transwell and wound healing assays. NSCLC xenograft models were used to confirm oncogenic function of IL-11 in vivo. Immunohistochemical staining and western blot assay were performed to detect epithelial–mesenchymal transition (EMT) markers and cell signaling pathway alterations. Eighteen NSCLC patients and 5 normal lung samples were collected together with data from an online database to determine the link between IL-11 expression and malignant progression. Results: We observed that IL-11 was upregulated in NSCLC samples compared with normal tissue samples and correlated with poor prognosis. Data from in vitro and in vivo models indicated that IL-11 promotes cell proliferation and tumorigenesis. Cell migration and invasion were also enhanced by IL-11. Epithelial–mesenchymal transition (EMT) was also observed after IL-11 incubation. Furthermore, IL-11 activated AKT and STAT3 in our experimental models. In addition, we observed that hypoxia induced IL-11 expression in NSCLC cells. Deferoxamine (DFX) or dimethyloxalylglycine (DMOG) induced hypoxia-inducible factor 1-alpha (HIF1α) upregulation, which enhanced IL-11 expression in NSCLC cells. Conclusions: Taken together, our results indicate that IL-11 is an oncogene in NSCLC, and elucidating the mechanism behind it may provide insights for NSCLC treatment.


Tumor Biology ◽  
2014 ◽  
Vol 35 (10) ◽  
pp. 9777-9785 ◽  
Author(s):  
Ji Zhou ◽  
Hui Bi ◽  
Ping Zhan ◽  
Cunjie Chang ◽  
Chunhua Xu ◽  
...  

2016 ◽  
Vol 11 (6) ◽  
pp. 3753-3760 ◽  
Author(s):  
YUNFEI LIAO ◽  
JIE GU ◽  
YONGBING WU ◽  
XIANG LONG ◽  
DI GE ◽  
...  

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