Distinct Role of Macrophages in Different Tumor Microenvironments

Lewis, Claire E.; Pollard, Jeffrey W.

doi:10.1158/0008-5472.can-05-4005

Cited by 1,969 publications

(1,806 citation statements)

References 69 publications

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“…The same situation is also found in human endometrial and breast cancers [77,78]. This recruitment of macrophages in this tumor microenvironment is dependent on CSF-1 (promoting the macrophage trophic phenotype) and also mediated by IL-4 and IL-10 (leading to immunosuppressive phenotype of macrophages) [79][80][81].…”

Section: Adenosine and Macrophage Interaction In Tumor Microenvironmentsupporting

confidence: 58%

Adenosine as an endogenous immunoregulator in cancer pathogenesis: where to go?

Kumar

2012

Purinergic Signalling

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Cancer is a chronic disease and its pathogenesis is well correlated with infection and inflammation. Adenosine is a purine nucleoside, which is produced under metabolic stress like hypoxic conditions. Acute or chronic inflammatory conditions lead to the release of precursor adenine nucleotides (adenosine triphosphate (ATP), adenosien diphosphate (ADP) and adenosine monophosphate (AMP)) from cells, which are extracellularly catabolized into adenosine by extracellular ectonucleotidases, i.e., CD39 or nucleoside triphosphate dephosphorylase (NTPD) and CD73 or 5′-ectonucleotidase. It is now well-known that adenosine is secreted by cancer as well as immune cells during tumor pathogenesis under metabolic stress or hypoxia. Once adenosine is released into the extracellular environment, it exerts various immunomodulatory effects via adenosine receptors (A 1 , A 2A , A 2B , and A 3 ) expressed on various immune cells (i.e., macrophages, myeloid-derived suppressor cells (MDSCs), natural killer (NK) cells, dendritic cells (DCs), T cells, regulatory T cell (T regs ), etc.), which play very important roles in the pathogenesis of cancer. This review is intended to summarize the role of inflammation and adenosine in the immunopathogenesis of tumor along with regulation of tumor-specific immune response and its modulation as an adjunct approach to tumor immunotherapy.

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Section: Adenosine and Macrophage Interaction In Tumor Microenvironmentsupporting

confidence: 58%

Adenosine as an endogenous immunoregulator in cancer pathogenesis: where to go?

Kumar

2012

Purinergic Signalling

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“…Inflammation often collaborates with environmental exposures, such as dietary derived toxins, to increase cancer risk even further 132 . The molecular mechanisms that underlie the pathogenesis of inflammation-associated cancer are complex, and involve both the innate and adaptive immune systems 3,133,134,135 . Although viral oncogenes can contribute directly to neoplastic transformation, neither infection nor pathogen-encoded oncogenes are required for inflammatory cells to induce cancer 136 .…”

Section: Box 1 | Molecular Mechanisms Of Inflammation-induced Cancersmentioning

confidence: 99%

“…Therefore, they might facilitate epithelial cell invasion into the stromal and vasculature compartments and, ultimately, the metastasis of tumour cells 133,134 . In another mechanism, the disruption of cytokine production and regulation, including cytokine deficiencies, lead to increased inflammation and cancer, whether in response to infection with a commensal organism or to chemical carcinogens 139 .…”

Section: Box 1 | Molecular Mechanisms Of Inflammation-induced Cancersmentioning

confidence: 99%

Inflammation in prostate carcinogenesis

et al. 2007

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About 20% of all human cancers are caused by chronic infection or chronic inflammatory states. Recently, a new hypothesis has been proposed for prostate carcinogenesis. It proposes that exposure to environmental factors such as infectious agents and dietary carcinogens, and hormonal imbalances lead to injury of the prostate and to the development of chronic inflammation and regenerative 'risk factor' lesions, referred to as proliferative inflammatory atrophy (PIA). By developing new experimental animal models coupled with classical epidemiological studies, genetic epidemiological studies and molecular pathological approaches, we should be able to determine whether prostate cancer is driven by inflammation, and if so, to develop new strategies to prevent the disease. NIH Public Access Author ManuscriptNat Rev Cancer. Author manuscript; available in PMC 2013 January 23. $watermark-text $watermark-text $watermark-textProstate cancer is the most common non-cutaneous malignant neoplasm in men in Western countries, responsible for the deaths of approximately 30,000 men per year in the United States 1 . The number of afflicted men is increasing rapidly as the population of males over the age of 50 grows worldwide. Therefore, finding strategies for the prevention of prostate cancer is a crucial medical challenge. As men in South East Asian countries have a low incidence of prostate cancer that increases rapidly after immigration to the West, this disease is not an intrinsic feature of ageing. The pathogenesis of prostate cancer reflects both hereditary and environmental components. What are the environmental factors and genetic variations that have produced such an epidemic of prostate cancer? Approximately 20% of all human cancers in adults result from chronic inflammatory states and/or chronic inflammation 2-4 (BOX 1), which are triggered by infectious agents or exposure to other environmental factors, or by a combination thereof. There is also emerging evidence that inflammation is crucial for the aetiology of prostate cancer. This evidence stems from epidemiological, histopathological and molecular pathological studies. The objective of this Review is to take a multidisciplinary approach to present and analyse such studies. Because several reviews related to these topics have been published [5][6][7] , here we will focus on new findings and ideas with the purpose of sparking innovative areas of investigation that might ultimately lead to the prevention of prostate cancer. Enigmas in the aetiology of prostate cancerAs in other cancers, prostate cancer develops through the accumulation of somatic genetic and epigenetic changes, resulting in the inactivation of tumour-suppressor genes and caretaker genes, and the activation of oncogenes 8,9 (TABLE 1). There is also evidence for an underlying genetic instability that might facilitate tumour progression 10,11 . Although these genetic and epigenetic changes are crucial for our understanding of 'how' prostate cancer arises, another key remaining question is 'why'...

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“…Indeed, macrophages control osteogenesis from mesenchymal stem cells, mechanism dependent on Oncostatin M signaling. The role of macrophages present in the vicinity of tumor cells, named "Tumor-Associated Macrophages" (TAMs), has been extensively studied [61][62][63]. [67].…”

Section: Osteosarcoma Cells Modulate the Balance Between Pro-and Antimentioning

confidence: 99%