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Tumor Microenvironment in Diffuse Large B-Cell Lymphoma: Role and Prognosis.
Analytical Cellular Pathology ( IF 2.6 ) Pub Date : 2019-12-16 , DOI: 10.1155/2019/8586354
Alexandra Ioana Cioroianu 1 , Patricia Irina Stinga 1 , Liana Sticlaru 1 , Mirela Daniela Cioplea 1 , Luciana Nichita 1, 2 , Cristiana Popp 1 , Florica Staniceanu 2
Affiliation  

Diffuse large B-cell lymphoma (DLBCL) represents 30-40% of all non-Hodgkin lymphomas (NHL) and is a disease with an aggressive behavior. Because about one-third of DLBCL patients will be refractory or resistant to standard therapy, several studies focused on identification of new individual prognostic and risk stratification biomarkers and new potential therapeutic targets. In contrast to other types of cancers like carcinomas, where tumor microenvironment was widely investigated, its role in DLBCL pathogenesis and patient survival is still poorly understood, although few studies had promising results. The composition of TME and its interaction with neoplastic cells may explain the role of several genes (beta2-microglobulin gene, CD58 gene), receptor-like programmed cell death-1 (PD-1) and its ligand (PD-L1), or other cell components (Treg) in tumor evasion of immune surveillance, resulting in tumor progression. Also, it was found that “gene expression profile” of the microenvironmental cells, the phenotype of tumor-associated macrophages (TAM), the expression of matricellular proteins like SPARC and fibronectin, the overexpression of several types of matrix metalloproteinases (MMPs) like MMP-2 and MMP-9, or the tissue inhibitors of matrix metalloproteinases (TIMPs) may lead to a favorable or adverse outcome. With this review, we try to highlight the influence of microenvironment components over lymphoid clone progression and their prognostic impact in DLBCL patients.

中文翻译:

弥漫性大B细胞淋巴瘤中的肿瘤微环境:作用和预后。

弥漫性大B细胞淋巴瘤(DLBCL)占所有非霍奇金淋巴瘤(NHL)的30-40%,是一种具有侵略性行为的疾病。由于约有三分之一的DLBCL患者对标准治疗无效或耐药,因此有几项研究侧重于鉴定新的个体预后和危险分层生物标志物以及新的潜在治疗靶标。与其他类型的癌症(如癌症)相比,肿瘤的微环境被广泛研究,与此相反,尽管很少有研究显示有希望的结果,但其在DLBCL发病机理和患者生存中的作用仍知之甚少。TME的组成及其与肿瘤细胞的相互作用可能解释了几种基因(β2-微球蛋白基因,CD58基因),受体样程序性细胞死亡1(PD-1)及其配体(PD-L1)的作用,或其他细胞成分(Treg)在逃避肿瘤的免疫监视下,导致肿瘤进展。此外,还发现微环境细胞的“基因表达谱”,肿瘤相关巨噬细胞(TAM)的表型,诸如SPARC和纤连蛋白的基质细胞蛋白的表达,诸如MMP的几种类型的基质金属蛋白酶(MMP)的过表达-2和MMP-9或基质金属蛋白酶(TIMPs)的组织抑制剂可能导致有利或不利的结果。通过这篇综述,我们试图强调微环境成分对淋巴样克隆进展的影响及其对DLBCL患者的预后影响。肿瘤相关巨噬细胞(TAM)的表型,诸如SPARC和纤连蛋白的基质细胞蛋白的表达,诸如MMP-2和MMP-9的几种类型的基质金属蛋白酶(MMPs)的过表达或基质金属蛋白酶(TIMPs)的组织抑制剂)可能会导致有利或不利的结果。通过这篇综述,我们试图强调微环境成分对淋巴样克隆进展的影响及其对DLBCL患者的预后影响。肿瘤相关巨噬细胞(TAM)的表型,诸如SPARC和纤连蛋白的基质细胞蛋白的表达,诸如MMP-2和MMP-9的几种类型的基质金属蛋白酶(MMPs)的过表达或基质金属蛋白酶(TIMPs)的组织抑制剂)可能会导致有利或不利的结果。通过这篇综述,我们试图强调微环境成分对淋巴样克隆进展的影响及其对DLBCL患者的预后影响。
更新日期:2019-12-16
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