Inflammation markers in cutaneous melanoma - edgy biomarkers for prognosis - PubMed (original) (raw)

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Inflammation markers in cutaneous melanoma - edgy biomarkers for prognosis

Monica Neagu et al. Discoveries (Craiova). 2015.

Abstract

There is a fine balance between inflammation and tumorigenesis. While environmentally induced inflammatory condition can precede a malignant transformation, in other cases an oncogenic change of unknown origin can induce an inflammatory microenvironment that promotes the development of tumors. Regardless of its origin, maintaining the inflammation milieu has many tumor-promoting effects. As a result, inflammation can aid the proliferation and survival of malignant cells, can promote angiogenesis and metastasis, can down-regulate innate/adaptive immune responses, and can alter responses to hormones and chemotherapeutic agents. There is an abundance of studies unveiling molecular pathways of cancer-related inflammation; this wealth of information brings new insights into biomarkers domain in the diagnosis and treatment improvement pursue. In cutaneous tissue there is an established link between tissue damage, inflammation, and cancer development. Inflammation is a self-limiting process in normal healthy physiological conditions, while tumorigenesis is a complex mechanism of constitutive pathway activation. Once more, in cutaneous melanoma, there is an unmet need for inflammatory biomarkers that could improve prognostication. Targeting inflammation and coping with the phenotypic plasticity of melanoma cells represent rational strategies to specifically interfere with metastatic progression. We have shown that there is a prototype of intratumor inflammatory infiltrate depicting a good prognosis, infiltrate that is composed of numerous T cells CD3+, Langerhans cells, few/absent B cells CD20+ and few/absent plasma cells. Circulating immune cells characterized by phenotype particularities are delicately linked to the stage melanoma is diagnosed in. Hence circulatory immune sub-populations, with activated or suppressor phenotype would give the physician a more detailed immune status of the patient. A panel of tissue/circulatory immune markers can complete the immune status, can add value to the overall prognostic of the patient and, as a result direct/redirect the therapy choice. The future lies within establishing low-cost, affordable/available, easily reproducible assays that will complete the pre-clinical parameters of the patient.

Keywords: circulatory immune cells; inflammation; melanoma; tissue biomarkers.

Copyright: © 2015, Neagu et al. and Applied Systems.

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Conflict of interest statement

Conflict of interests: The authors declare no conflict of interest.

Figures

Figure 1

Figure 1. Acute and chronic skin inflammation cascade

**A. The initial skin injury triggers first intravascular processes that activate neutrophils’ adhesion and transmigration. Resident macrophages and mastocytes release pro-inflammatory and chemoattractant factors; B. Lymphocytes and monocytes have increased adhesion capacities and further transmigrate into extravascular space. Transmigrated cells and resident macrophages secrete pro-inflammatory and chemoattractants factors, stimulating collagen production and perpetuating the inflammatory response.The HIV-1 PR is shown as a cartoon in green. The key residue mutations contributing to flap dynamics are shown in red. The catalytic aspartic acid residues are shown in blue. Darunavir is bound to the active site in cyan.

Figure 2

Figure 2. Acute and chronic inflammation elements that are linked to tumorigenesis

**A. T and B lymphocytes secrete factors that induce M1 macrophage phenotype, enhance innate immunity, CTL-mediated destruction, activation of the antigen presenting capacity and NK cell activation. All these processes have a potent anti-tumorigenesis action; B. T and B lymphocytes secrete factors that induce M2 macrophage phenotype, enhance myeloid suppressor activity, reduce CTL activity, decrease antigen presenting capacity and NK cell activity. All these processes have a potent pro-tumorigenesis action.

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References

    1. Lindlahr Henry. Nature Cure: Philosophy & Practice Based on the Unity of Disease & Cure. The Nature Cure Publishing Company; 1922.
    1. Acute and Chronic Inflammation. Ward Peter A., Ayoub Samir S. Fundamentals of Inflammation :1-16.
    1. Inflammation and breast cancer. Balancing immune response: crosstalk between adaptive and innate immune cells during breast cancer progression. DeNardo David G, Coussens Lisa M. Breast Cancer Research. 2007;9(4) - PMC - PubMed
    1. Cancer-related inflammation. Mantovani Alberto, Allavena Paola, Sica Antonio, Balkwill Frances. Nature. 2008;454(7203):436–44. - PubMed
    1. Chronic inflammation, the tumor microenvironment and carcinogenesis. Gonda Tamas A, Tu Shuiping, Wang Timothy C. Cell cycle (Georgetown, Tex.) 2009;8(13):2005–13. - PubMed

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