Tumour-associated mast cells in classical Hodgkin's lymphoma: correlation with histological subtype, other tumour-infiltrating inflammatory cell subsets and outcome
Tumour-associated mast cells in classical Hodgkin's lymphoma: correlation with histological subtype, other tumour-infiltrating inflammatory cell subsets and outcome
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DOI：
10.1111/ejh.12583
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发表时间：
2016-03-01
影响因子：
3.1
通讯作者：
d'Amore, Francesco
中科院分区：
文献类型：
--
作者：
Andersen, Maja D.;Kamper, Peter;d'Amore, Francesco
经典型霍奇金淋巴瘤（cHL）的肿瘤微环境的特征是在非肿瘤性旁观者细胞（包括肥大细胞）的异质背景中存在少量肿瘤性霍奇金和Reed-Sternberg细胞。据报道，cHL中浸润肥大细胞的数量与不良预后相关。我们使用免疫组化评估cHL组织微阵列中肿瘤浸润肥大细胞的程度，并将其与一组接受均匀治疗的霍奇金病患者的临床病理特征和预后相关。高度的肿瘤肥大细胞与结节性硬化（NS）亚型组织学相关（P=0.0002）。此外，肥大细胞的数量与CD 68+和CD 163+巨噬细胞的数量呈负相关（分别为P=0.0001和P=0.003），与颗粒酶+细胞毒性细胞的数量呈负相关（P=0.004）。肥大细胞浸润程度不是结节硬化型cHL的预后因素。相比之下，在混合细胞型cHL中，大量瘤内肥大细胞与总体（P=0.03）和无事件生存期（P=0.01）方面的结局显著较差相关。进一步的研究是必要的生物学机制，这种不良后果及其可能的治疗意义。
The tumour microenvironment in classical Hodgkin's lymphoma (cHL) is characterised by a minor population of neoplastic Hodgkin and Reed-Sternberg cells within a heterogeneous background of non-neoplastic bystanders cells, including mast cells. The number of infiltrating mast cells in cHL has been reported to correlate with poor prognosis. We used immunohistochemistry to assess the degree of tumour-infiltrating mast cells in cHL tissue microarrays and correlated this with clinico-pathological features and prognosis in a cohort of homogeneously treated patients with Hodgkin's disease. A high degree of tumour mast cells was associated with nodular sclerosis (NS) subtype histology (P=0.0002). Moreover, the number of mast cells was inversely correlated with the numbers of CD68+ and CD163+ macrophages (P=0.0001 and P=0.003, respectively) and with the number of granzyme+ cytotoxic cells (P=0.004). The degree of mast cell infiltration was not a prognostic factor in cHL of nodular sclerosis subtype. In contrast, in mixed cellularity cHL a high number of intratumoral mast cells correlated with significantly poorer outcome both in terms of overall (P=0.03) and event-free survival (P=0.01). Further studies are warranted into the biological mechanisms underlying this adverse outcome and their possible therapeutic implications.