Density of Tumor-Associated Macrophages Correlates with Lymph Node Metastasis in Papillary Thyroid Carcinoma

Wei, Qing; Fang, Weiyuan; Ye, Lei; Shen, Liyun; Zhang, Xiaofang; Fei, Xiaochun; Chen, Xi; Wang, Weiqing; Li, Xiaoying; Xiao, Jiaqi; Ning, Guang

doi:10.1089/thy.2011.0452

Cited by 107 publications

(107 citation statements)

References 29 publications

(30 reference statements)

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“…Ryder et al (2008) first demonstrated that high density of macrophages was associated with poor clinical outcome in advanced thyroid cancer, while following data have shown conflicting results (Ryder et al 2008, Cunha et al 2012, Qing et al 2012, Fang et al 2014. Meanwhile, recent experimental studies have been more focused on the pro-tumorigenic roles of macrophages.…”

Section: Discussionmentioning

confidence: 99%

“…In thyroid cancers, a few epidemiologic studies have shown that high TAM densities were associated with poor pathologic subtypes, bigger tumor size, or the presence of LN metastasis (Ryder et al 2008, Qing et al 2012. Recently, several studies have been demonstrated possible molecular mechanisms of macrophage actions in PTCs, such as CXCL8 (Fang et al 2014) or CSF1 (Ryder et al 2013).…”

Section: Introductionmentioning

confidence: 99%

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CXCL16 signaling mediated macrophage effects on tumor invasion of papillary thyroid carcinoma

Cho¹,

Kim²,

Sun³

et al. 2015

Endocrine-Related Cancer

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Macrophages in tumor microenvironment have pivotal roles in tumor growth, metastasis, and angiogenesis. We investigated the interacting mechanism of macrophage actions in human papillary thyroid cancer (PTC). Co-cultures of macrophage/PTC significantly increased the cancer cell migration potentials, compared with the PTC culture alone. Treatment of conditioned medium (CM) of macrophage/PTC co-cultures enhanced cell invasions in 3D invasion assay. Cytokine array analysis demonstrated that CM of macrophage/PTC co-cultures contained a high level of CXCL16, while it was not found in CM of PTC culture alone. Treatment with CXCL16 enhanced the cell migration potentials in PTC cells, and blocking CXCL16 signaling using anti-CXCL16 antibody or metalloproteinase inhibitor (TAPI2) attenuated macrophagemediated enhancement of PTC cell migration potentials. In PTC cells, CXCL16 treatment or co-cultures with macrophages increased Akt phosphorylation, and these macrophagedependent increases of Akt phosphorylation was inhibited by anti-CXCL16 antibody. Moreover, Akt inhibitor attenuated macrophage-mediated increases of PTC cell migration potential. In macrophages, treatment of macrophage/PTC co-cultured CMs up-regulated CD163, Il10, and CD206, which were attenuated by anti-CXCL16 antibody treatment. Finally, CXCR6 and CXCL16 expressions were evaluated by immunohistochemical staining with a thyroid tissue microarray including 136 PTC. CXCR6 expressions showed positive correlation with the density of CD163 C macrophages and associated with lymph node metastasis. In conclusion, CXCL16 signaling partly mediated macrophage actions on PTC tumor cell invasion and also changed the macrophage phenotypes into M2-macrophages in PTC tumor microenvironment. These data suggested that CXCL16 signaling, a bidirectional player in macrophage-associated tumor microenvironment, might be a potential therapeutic target of human PTC.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

CXCL16 signaling mediated macrophage effects on tumor invasion of papillary thyroid carcinoma

Cho¹,

Kim²,

Sun³

et al. 2015

Endocrine-Related Cancer

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“…The frequency of the HRAS variant did not differ among PTC subtypes (P=0.95). There were no associations between the HRAS variant and age, sex, tumor size, encapsulation, multifocality/intrathyroidal spread, Tumor-Node-Metastasis stage (22), thyroid nodule status, Hashimoto history, BRAF mutation or PTC subtype (all P>0.05; Table III). There were significant differences in the number of BRAF mutations among the different subtypes (P=0.041; Table IV).…”

Section: Single-stranded Conformational Polymorphism Analysis (Sscp) mentioning

confidence: 96%

Identification of a novel HRAS variant and its association with papillary thyroid carcinoma

Dou

Zhang

et al. 2018

Oncol Lett

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Abstract. HRas proto-oncogene (HRAS) is one of the most commonly mutated genes in thyroid cancer, with mutations frequently occurring in the follicular and Hurthle cell subtypes. However, the contribution of mutations in HRAS to papillary thyroid carcinoma (PTC) progression and the tall-cell variant (TCV) is poorly understood. The aim of the present study was to investigate the somatic genetic variants present in HRAS in patients with PTC, and to investigate the association of these mutations with PTC. The present study is a retrospective case-control study using tumor samples collected from 139 patients with PTC and blood samples from 195 healthy individuals. All patient samples were screened for mutations in 'hotspot' regions of HRAS and B-raf proto-oncogene (BRAF) by single-stranded conformational polymorphism analysis, followed by direct sequencing. A novel variant (IVS1-82del gctgggcctggg) in the HRAS 5'-untranslated region was identified. There was no difference in age or sex of patients with PTC and the healthy controls; however, the HRAS variant was more frequently detected in PTC tissue than in the healthy control samples (37 vs. 26%, P=0.04). There was no association between the HRAS variant and age, sex, tumor size, encapsulation, multifocality/intra-thyroidal spread, Tumor-Node-Metastasis stage, history of Hashimoto's disease, BRAF V600E mutation or PTC subtype (all P>0.05). There were differences of BRAF V600E distribution among different subtypes (χ 2 =6.390, P=0.041). HRAS variant co-occurring with the BRAF V600E mutation accounted for 31.6% of the total number (P=0.196). Therefore, this novel variant of HRAS (IVS1-82del gctgggcctggg) may be associated with PTC; however, larger scale studies are required to assess the contribution of this novel HRAS variant to PTC progression.

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“…In addition, Csf-/-BRAF transgenic mice displayed a reduction in tumor growth. 14 Accordingly, TAMs purified from human PTC displayed a higher expression of IL-10 and CD206 compared to peripheral blood monocytes 71 and promoted invasiveness of TC cell lines in vitro through to the production of CXCL8/IL-8. 45 …”

Section: Immune Cells In Tc Microenvironmentmentioning

confidence: 99%

The immune network in thyroid cancer

2016

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The immune system plays critical roles in tumor prevention, but also in its initiation and progression. Tumors are subjected to immunosurveillance, but cancer cells generate an immunosuppressive microenvironment that favors their escape from immune-mediated elimination. During chronic inflammation, immune cells can contribute to the formation and progression of tumors by producing mitogenic, prosurvival, proangiogenic and lymphangiogenic factors. Thyroid cancer is the most frequent type of endocrine neoplasia and is the most rapidly increasing cancer in the US. In this review, we discuss recent findings on how different immune cells and mediators can contribute to thyroid cancer development and progression.

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Density of Tumor-Associated Macrophages Correlates with Lymph Node Metastasis in Papillary Thyroid Carcinoma

Cited by 107 publications

References 29 publications

CXCL16 signaling mediated macrophage effects on tumor invasion of papillary thyroid carcinoma

CXCL16 signaling mediated macrophage effects on tumor invasion of papillary thyroid carcinoma

Identification of a novel HRAS variant and its association with papillary thyroid carcinoma

The immune network in thyroid cancer

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