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Journal Article
Research Support, Non-U.S. Gov't
Review
Cutaneous B-cell lymphoma.
Dermatologic Clinics 1985 October
The various morphologic and functional subtypes of nodal B-cell lymphomas can also be found in the skin. These reflect the various steps of lymphocyte differentiation including maturation from the pre-B lymphocyte to the well-differentiated B2 lymphocyte or plasma cell in the peripheral blood. The subtypes of cutaneous B-cell lymphomas have been discussed (Kiel classification); the percentages indicate the frequencies of the subtypes among a total of 736 cutaneous lymphomas of both T-cell and B-cell origin: Lymphocytic lymphoma (7 per cent). Immunoglobulin-producing lymphomas, including the rate plasmacytoma of the skin, lymphoplasmacytoid immunocytoma, which represents the largest group of cutaneous B-cell lymphoma (12 per cent), and immunoblastic lymphoma, which is the most aggressive form in this group (8 per cent). Cutaneous B-cell lymphoma arising from or related to follicular center cells, including centrocytic lymphoma (7 per cent), mantle-cell lymphoma, centroblastic/centrocytic lymphoma (6 per cent), the highly malignant centroblastic lymphoma (4 per cent), and lymphoblastic lymphoma, Burkitt type. The Ann Arbor staging system is not applicable to cutaneous B-cell lymphoma; therefore, a TNM staging system has been proposed. The diagnosis of cutaneous B-cell lymphoma is based primarily on cytomorphologic features. Differentiation of cutaneous B-cell lymphoma from pseudolymphoma of the skin cannot be based on a single criterion; a spectrum of characteristic features must be evaluated. Analysis of the infiltrating cells in cutaneous B-cell lymphoma using monoclonal antibodies demonstrates that the proliferation of the neoplastic clone is accompanied by a mixture of accessory cells of various origins, including T cells, macrophages, and dendritic reticulum cells. As in nodal B-cell lymphomas, several factors may be involved in the generation of cutaneous B-cell lymphoma, including persistent antigenic stimulation and loss of regulatory mechanisms for lymphocyte proliferation and differentiation in conjunction with environmental and other factors.
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