Phagocytes as Corrupted Policemen in Cancer-Related Inflammation

Bonavita, Eduardo; Galdiero, Maria Rosaria; Jaillon, Sébastien; Mantovani, Alberto

doi:10.1016/bs.acr.2015.04.013

Cited by 92 publications

(73 citation statements)

References 182 publications

(224 reference statements)

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“…Moreover, TAMs provide a supportive niche for metastatic tumor cells at distant sites by secreting inflammatory factors, such as IL1 [4]. In addition, ROS and nitrogen intermediates generated by TAMs contribute to genetic instability of cancer cells [20], a hallmark of cancer that tremendously limits the effectiveness of anti-tumor chemotherapies.…”

Section: Role Of Macrophages In Cancermentioning

confidence: 99%

The Role of Tumor-Associated Macrophages in Colorectal Carcinoma Progression

Zhong¹,

Chen²,

Yang³

2018

Cell Physiol Biochem

109

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Tumor-associated macrophages (TAMs) are one of the most abundant immune cells in the tumor microenvironment, and they play a pivotal role in prompting the various tumor growth. However, the role of TAMs in colorectal carcinoma (CRC) is controversial, because a few papers report that TAMs is beneficial to CRC patients. In this review, we discuss the good or bad roles of TAMs in CRC progression. Interestingly, recent studies provide strong evidence that TAMs facilitate CRC growth, but do not exert tumor suppressive activities. TAMs can stimulate CRC growth by altering extracellular matrix remodeling, tumor metabolism, angiogenesis, as well as the tumor microenvironment. Therefore, TAMs could serve as a target for CRC therapeutic treatment.

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Section: Role Of Macrophages In Cancermentioning

confidence: 99%

The Role of Tumor-Associated Macrophages in Colorectal Carcinoma Progression

Zhong¹,

Chen²,

Yang³

2018

Cell Physiol Biochem

109

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“…In the sporadic intestinal carcinogenesis model, we noted decreased macrophages in both the adenomas and uninvolved intestine associated with CCR6 deficiency. 4 As a tumor-promoting effect of macrophages is supported by several lines of evidence, [12][13][14] we suspected that CCR6 may mediate enhanced adenoma growth through recruitment of macrophages. Thus, we investigated whether CCR6 deficiency decreases infiltrating macrophages in the transplanted tumor, Figure 1.…”

Section: Deficiency Of Host Ccr6 Decreases Infiltration Of Macrophagementioning

confidence: 86%

“…Other molecules such as colony-stimulating factor 2 (CSF-2, also known as granulocyte-macrophage colony-stimulating factor (GM-CSF)), vascular endothelial growth factor (VEGF), Transforming growth factor b (TGF-b), and CXCL12 (also known as stromal cell-derived factor 1 (SDF-1)) have also been shown to be involved in the recruitment of tumor macrophages. [12][13][14] The role of CCL20-CCR6 interactions in monocyte/macrophage recruitment is not well established. In a model of breast cancer development related to expression of a polyoma virus gene, tumor macrophages were found to be decreased in tumors that developed in CCR6-deficient mice.…”

Section: Discussionmentioning

confidence: 99%

“…[12][13][14] Some studies relying on immunohistochemical staining of human colorectal cancers, in fact, indicate that macrophages along the tumor margin [31][32][33] and macrophages expressing VEGF 34 are associated with a good prognosis. Others have suggested that macrophages in colorectal cancer may have co-stimulatory functions in antitumor immunity 35 or may be able to induce tumor cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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Stromal CCR6 drives tumor growth in a murine transplantable colon cancer through recruitment of tumor-promoting macrophages

et al. 2016

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Interactions between the inflammatory chemokine CCL20 and its receptor CCR6 have been implicated in promoting colon cancer; however, the mechanisms behind this effect are poorly understood. We have previously demonstrated that deficiency of CCR6 is associated with decreased tumor macrophage accumulation in a model of sporadic intestinal tumorigenesis. In this study, we aimed to determine the role of stromal CCR6 expression in a murine syngeneic transplantable colon cancer model. We show that deficiency of host CCR6 is associated with decreased growth of syngeneic CCR6-expressing colon cancers. Colon cancers adoptively transplanted into CCR6-deficient mice have decreased tumor-associated macrophages without alterations in the number of monocytes in blood or bone marrow. CCL20, the unique ligand for CCR6, promotes migration of monocytes in vitro and promotes accumulation of macrophages in vivo. Depletion of tumor-associated macrophages decreases the growth of tumors in the transplantable tumor model. Macrophages infiltrating the colon cancers in this model secrete the inflammatory mediators CCL2, IL-1a, IL-6 and TNFa. Ccl2, Il1a and Il6 are consequently downregulated in tumors from CCR6-deficient mice. CCL2, IL-1a and IL-6 also promote proliferation of colon cancer cells, linking the decreased macrophage migration into tumors mediated by CCL20-CCR6 interactions to the delay in tumor growth in CCR6-deficient hosts. The relevance of these findings in human colon cancer is demonstrated through correlation of CCR6 expression with that of the macrophage marker CD163 as well as that of CCL2, IL1a and TNFa. Our findings support the exploration of targeting the CCL20-CCR6 pathway for the treatment of colon cancer.

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“…Indeed, inflammatory cells such as tumor-associated macrophages (TAMs) and several soluble factors are fundamental components of the tumor microenvironment and mediate tumor-promoting effects [252, 253]. The recruitment of monocytes from peripheral circulation and their subsequent differentiation to TAMs is an essential step in establishing the tumor microenvironment, which has several features of a chronic inflammatory state.…”

Section: Inflammationmentioning

confidence: 99%

The biology of uveal melanoma

Amaro

Gangemi

Piaggio

et al. 2017

Cancer Metastasis Rev

191

193

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Uveal melanoma (UM), a rare cancer of the eye, is distinct from cutaneous melanoma by its etiology, the mutation frequency and profile, and its clinical behavior including resistance to targeted therapy and immune checkpoint blockers. Primary disease is efficiently controlled by surgery or radiation therapy, but about half of UMs develop distant metastasis mostly to the liver. Survival of patients with metastasis is below 1 year and has not improved in decades. Recent years have brought a deep understanding of UM biology characterized by initiating mutations in the G proteins GNAQ and GNA11. Cytogenetic alterations, in particular monosomy of chromosome 3 and amplification of the long arm of chromosome 8, and mutation of the BRCA1-associated protein 1, BAP1, a tumor suppressor gene, or the splicing factor SF3B1 determine UM metastasis. Cytogenetic and molecular profiling allow for a very precise prognostication that is still not matched by efficacious adjuvant therapies. G protein signaling has been shown to activate the YAP/TAZ pathway independent of HIPPO, and conventional signaling via the mitogen-activated kinase pathway probably also contributes to UM development and progression. Several lines of evidence indicate that inflammation and macrophages play a pro-tumor role in UM and in its hepatic metastases. UM cells benefit from the immune privilege in the eye and may adopt several mechanisms involved in this privilege for tumor escape that act even after leaving the niche. Here, we review the current knowledge of the biology of UM and discuss recent approaches to UM treatment.

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Phagocytes as Corrupted Policemen in Cancer-Related Inflammation

Cited by 92 publications

References 182 publications

The Role of Tumor-Associated Macrophages in Colorectal Carcinoma Progression

The Role of Tumor-Associated Macrophages in Colorectal Carcinoma Progression

Stromal CCR6 drives tumor growth in a murine transplantable colon cancer through recruitment of tumor-promoting macrophages

The biology of uveal melanoma

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