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Tumour‐associated mast cells in classical Hodgkin's lymphoma: correlation with histological subtype, other tumour‐infiltrating inflammatory cell subsets and outcome
Author(s) -
Andersen Maja D.,
Kamper Peter,
Nielsen Patricia S.,
Bendix Knud,
RiberHansen Rikke,
Steiniche Torben,
HamiltonDutoit Stephen,
Clausen Michael,
d'Amore Francesco
Publication year - 2016
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/ejh.12583
Subject(s) - nodular sclerosis , cd68 , pathology , mast cell , lymphoma , medicine , immunophenotyping , population , granzyme b , immunohistochemistry , cd163 , immune system , biology , immunology , t cell , flow cytometry , macrophage , hodgkin lymphoma , biochemistry , environmental health , in vitro
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 CD 68+ and CD 163+ 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.