Relationship of tumour-associated macrophages with poor prognosis in Wilms’ tumour

Tian, Kaixuan; Wang, Xiaoqing; Wu, Yidi; Wu, Xiangyu; Du, Guiqiang; Liu, Wei; Wu, Renyi

doi:10.1016/j.jpurol.2020.03.016

Cited by 19 publications

(17 citation statements)

References 27 publications

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“…Urol. 2020 29 immune infiltration (M1 and M2-type TAM↓∗) IHC, IF, western blot 61 Vakkila et al. Clinical Cancer Res.…”

Section: Methodsmentioning

confidence: 99%

“…All studies underline the presence of an immunosuppressive microenvironment in Wilms tumor. 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 The cell infiltrate is usually detected in the stromal component of the tumor, and the most abundant cells are tumor-associated macrophages (TAMs). 19 , 24 , 25 , 29 There has been an attempt to correlate the presence of such cells to clinicopathological features of WT.…”

Section: Immune Cell Infiltrationmentioning

confidence: 99%

“…An increased ratio of M2/M1 correlated with disease progression from stage I to stage III, prognosis and unfavorable histology. 29 Thus, the macrophage infiltrate might be employed to refine the staging algorithm.…”

Section: Immune Cell Infiltrationmentioning

confidence: 99%

See 2 more Smart Citations

Systematic review of the immunological landscape of Wilms tumors

Palmisani

Kovar

Kager

et al. 2021

Molecular Therapy - Oncolytics

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Results of immunotherapy in childhood solid cancer have been so far, with the exception of neuroblastoma, quite disappointing. Lack of knowledge of the immune contexture of these tumors may have contributed to the failure of immunotherapies so far. Here, we systematically reviewed the literature regarding the immunology of Wilms tumor (WT), one of the most frequent pediatric solid tumors of the abdomen. In Wilms tumor patients the high cure rate of >90%, achieved by the combination of surgery and radio-chemotherapy, is at the expense of a high early and late toxicity. Moreover, treatment-resistant entities, such as diffuse anaplastic tumors or recurrent disease, still pose unsolved clinical problems. Successful immunotherapy could represent a novel and possibly less-toxic treatment option. Employing the PRISMA (Preferred Reporting Items for Systematic Review and Meta-Analysis) method of literature search, we analyzed the current knowledge of the immunological landscape of Wilms tumors in terms of tumor microenvironment, prognostic implications of single biomarkers, and immunotherapy response.

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“…Urol. 2020 29 immune infiltration (M1 and M2-type TAM↓∗) IHC, IF, western blot 61 Vakkila et al. Clinical Cancer Res.…”

Section: Methodsmentioning

confidence: 99%

Section: Immune Cell Infiltrationmentioning

confidence: 99%

See 1 more Smart Citation

Systematic review of the immunological landscape of Wilms tumors

Palmisani

Kovar

Kager

et al. 2021

Molecular Therapy - Oncolytics

View full text Add to dashboard Cite

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“…Knowing the various functions of M2 macrophage population, it is now generally accepted that TAMs promote tumor progression and metastasis by activating circuits that regulate tumor growth, adaptive immunity, anti-tumor immunity, stroma formation, and angiogenesis [ 32 , 35 , 41 , 42 , 43 , 44 , 45 ]. In a variety of human tumors, including breast, prostate, renal, bladder, lung, cervical carcinoma, glioma, lymphoma, and melanoma, a high number of TAMs infiltrating the tumor stroma is also associated with a higher incidence of metastasis and more aggressive types of cancer that eventually lead to a poor prognosis of the disease [ 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 ]. The transcription factor MYC is known to be involved in cell proliferation, apoptosis, tissue remodeling, angiogenesis, cell metabolism, and the production of both inflammatory and anti-inflammatory cytokines [ 54 , 55 , 56 , 57 ].…”

Section: Myc–a Key Player In the Tumor Microenvironment (Tme)mentioning

confidence: 99%

MYC as a Multifaceted Regulator of Tumor Microenvironment Leading to Metastasis

Meškytė

Keskas

Ciribilli

2020

IJMS

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The Myc family of oncogenes is deregulated in many types of cancer, and their over-expression is often correlated with poor prognosis. The Myc family members are transcription factors that can coordinate the expression of thousands of genes. Among them, c-Myc (MYC) is the gene most strongly associated with cancer, and it is the focus of this review. It regulates the expression of genes involved in cell proliferation, growth, differentiation, self-renewal, survival, metabolism, protein synthesis, and apoptosis. More recently, novel studies have shown that MYC plays a role not only in tumor initiation and growth but also has a broader spectrum of functions in tumor progression. MYC contributes to angiogenesis, immune evasion, invasion, and migration, which all lead to distant metastasis. Moreover, MYC is able to promote tumor growth and aggressiveness by recruiting stromal and tumor-infiltrating cells. In this review, we will dissect all of these novel functions and their involvement in the crosstalk between tumor and host, which have demonstrated that MYC is undoubtedly the master regulator of the tumor microenvironment. In sum, a better understanding of MYC’s role in the tumor microenvironment and metastasis development is crucial in proposing novel and effective cancer treatment strategies.

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“…6 High density of TAMs is associated with both poor prognosis and decreased survival in multiple cancer types. [7][8][9] Studies have corroborated that TAMs commonly function as pro-inflammatory or anti-inflammatory under TME stimulus where a pro-or anti-tumorigenic environment is created. TAMs are more prevalent in tumors of children with metastatic rather than locoregional NB.…”

Section: Introductionmentioning

confidence: 97%

FABP4 deactivates NF‐κB‐IL1α pathway by ubiquitinating ATPB in tumor‐associated macrophages and promotes neuroblastoma progression

Miao

Zhang

Tang

et al. 2021

Clinical & Translational Med

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Neuroblastoma (NB) is the most common and deadliest pediatric solid tumor. Targeting and reactivating tumor‐associated macrophages (TAMs) is necessary for reversing immune suppressive state and stimulating immune defense to exert tumoricidal function. However, studies on the function and regulation of TAMs in NB progression are still limited. Fatty acid binding protein 4 (FABP4) in TAMs was correlated with advanced clinical stages and unfavorable histology of NB. FABP4‐mediated macrophages increased migration, invasion, and tumor growth of NB cells. Mechanically, FABP4 could directly bind to ATPB to accelerate ATPB ubiquitination in macrophages. The consequently decreased ATP levels could deactivate NF‐κB/RelA‐IL1α pathway, which subsequently results in macrophages reprogrammed to an anti‐inflammatory phenotype. We also demonstrated that FABP4‐enhanced migration and invasion were significantly suppressed by IL1α blocking antibody. Furthermore, circulating FABP4 was also associated with the clinical stages of NB. Our findings suggest that FABP4‐mediated macrophages may promote proliferation and migration phenotypes in NB cells through deactivating NF‐κB‐IL1α pathway by ubiquitinating ATPB. This study reveals the pathologic and biologic role of FABP4‐mediated macrophages in NB development and exhibits a novel application of targeting FABP4 in macrophages for NB treatment.

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Relationship of tumour-associated macrophages with poor prognosis in Wilms’ tumour

Cited by 19 publications

References 27 publications

Systematic review of the immunological landscape of Wilms tumors

Systematic review of the immunological landscape of Wilms tumors

MYC as a Multifaceted Regulator of Tumor Microenvironment Leading to Metastasis

FABP4 deactivates NF‐κB‐IL1α pathway by ubiquitinating ATPB in tumor‐associated macrophages and promotes neuroblastoma progression

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