Neagu Monica, Constantin Carolina, Dumitrascu Georgiana Roxana, Lupu Andreea Roxana, Caruntu Constantin, Boda Daniel, Zurac Sabina
Immunobiology Laboratory, "Victor Babes" National Institute of Pathology and Biomedical Sciences, Bucharest, Romania.
Faculty of Biochemistry, University of Bucharest, Romania.
Discoveries (Craiova). 2015 Mar 27;3(1):e38. doi: 10.15190/d.2015.30.
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.
炎症与肿瘤发生之间存在微妙的平衡。虽然环境诱导的炎症状态可能先于恶性转化,但在其他情况下,不明来源的致癌变化可诱导促进肿瘤发展的炎症微环境。无论其起源如何,维持炎症环境具有许多促肿瘤作用。因此,炎症可促进恶性细胞的增殖和存活,促进血管生成和转移,下调先天/适应性免疫反应,并改变对激素和化疗药物的反应。有大量研究揭示了癌症相关炎症的分子途径;这些丰富的信息为追求诊断和治疗改善的生物标志物领域带来了新的见解。在皮肤组织中,组织损伤、炎症与癌症发展之间存在既定联系。在正常健康的生理条件下,炎症是一个自我限制的过程,而肿瘤发生是一个组成性途径激活的复杂机制。再一次,在皮肤黑色素瘤中,对可改善预后的炎症生物标志物仍有未满足的需求。针对炎症并应对黑色素瘤细胞的表型可塑性是特异性干扰转移进展的合理策略。我们已经表明,存在一种肿瘤内炎症浸润的原型,其预后良好,这种浸润由大量CD3 + T细胞、朗格汉斯细胞、少量/无CD20 + B细胞和少量/无浆细胞组成。以表型特殊性为特征的循环免疫细胞与黑色素瘤诊断的阶段密切相关。因此,具有激活或抑制表型的循环免疫亚群将为医生提供患者更详细的免疫状态。一组组织/循环免疫标志物可以完善免疫状态,为患者的整体预后增加价值,从而指导/重新指导治疗选择。未来在于建立低成本、可负担/可获得、易于重复的检测方法,以完善患者的临床前参数。