Premium
Epithelioid cell histiocytoma – histogenetic and kinetics analysis of dermal microvascular unit dendritic cell subpopulations
Author(s) -
Silverman Jeffrey S.,
Glusac Earl J.
Publication year - 2003
Publication title -
journal of cutaneous pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 75
eISSN - 1600-0560
pISSN - 0303-6987
DOI - 10.1034/j.1600-0560.2003.00094.x
Subject(s) - histiocyte , pathology , cd34 , cd31 , epithelioid cell , dendritic cell , stromal cell , cd68 , biology , chemistry , immunohistochemistry , microbiology and biotechnology , immunology , medicine , stem cell , antigen
Background: Epithelioid cell histiocytoma (ECH), also known as epithelioid fibrous histiocytoma, is a peculiar dermal tumor, which can mimic melanocytic, vascular, epithelial, or other histiocytic lesions. Thought to arise from dermal dendrocytes, most ECH contain approximately 50% FXIIIa + histiocytic dendrocytes, but not all lesional cells express FXIIIa. A putative fibroblastic component has not been characterized. Methods: We analyzed the differentiation and cell kinetics of dermal microvascular unit cells in 12 previously reported ECH using antibodies to FXIIIa, CD68 (KP1), CD34, CD117, CD31, smooth muscle actin, collagen type 1 aminopropeptide, and MIB‐1, using single and double immunostains. Results: In ECH, many variably sized CD34/CD31 + tumor vessels with actin + myopericytes were surrounded by epithelioid‐to‐dendritic cells of three types. About 5–80% were dendritic histiocytes that expressed FXIIIa but not CD31 or KP1. Fibroblasts, in some cases showing mild nuclear pleomorphism, were usually collagen type 1 + , but CD34 and actin – in 11/12 cases. One ‘early’ ECH had 40% CD34 + epithelioid cells, admixed with 50% FXIIIa + histiocytes. Most ECH had about 2–20% KP1 + , CD117 + mast cells. Mast cell numbers increased with FXIIIa + histiocyte numbers and the intensity of FXIIIa expression. MIB‐1/FXIIIa double‐labeling showed only rare cycling histiocytes, with numerous cycling fibroblasts and endothelial cells. Conclusions: Our findings support the impression that ECH is a vascular fibrous histiocytoma. The constituent cells appear to arise from the activation of resident microvascular CD34 + dermal fibroblasts and the accumulation of FXIIIa + dendritic stromal assembly histiocytes. The CD34 + cells appear to differentiate toward collagenous fibrocytes in association with histiocytes and mast cells in forming collagenous stroma and vessels. ECH is a tumor composed of all requisite cell types consistent with the origin from the dermal microvascular unit.