Department of Pathology, Colentina Clinical Hospital, 020125 Bucharest, Romania.
Faculty of Dental Medicine, University of Medicine and Pharmacy "Carol Davila", 020021 Bucharest, Romania.
Anal Cell Pathol (Amst). 2019 Dec 16;2019:8586354. doi: 10.1155/2019/8586354. eCollection 2019.
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.
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%,是一种具有侵袭性的疾病。由于约三分之一的 DLBCL 患者对标准治疗会产生耐药或抵抗,因此有几项研究集中在鉴定新的个体预后和风险分层生物标志物和新的潜在治疗靶点上。与其他类型的癌症(如癌)不同,后者的肿瘤微环境已被广泛研究,但它在 DLBCL 发病机制和患者生存中的作用仍知之甚少,尽管少数研究结果有希望。TME 的组成及其与肿瘤细胞的相互作用可以解释几个基因(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) 或其他细胞成分(Treg)在肿瘤逃避免疫监视中的作用,从而导致肿瘤进展。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、基质细胞蛋白(如 SPARC 和纤维连接蛋白)的表达、几种基质金属蛋白酶 (MMPs)(如 MMP-2 和 MMP-9)的过度表达,或基质金属蛋白酶组织抑制剂 (TIMPs) 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细胞克隆进展的影响及其对 DLBCL 患者预后的影响。