Abstract
Lymphomatoid papulosis (LyP) is a recurrent, multifocal cutaneous eruption characterized pathologically as an infiltration of large atypical cells surrounded by inflammatory cells (Macaulay, 1968). The large atypical cells resemble Reed Sternberg (RS) cells of Hodgkin disease (HD) (type A LyP cells), or Sézary cells of cutaneous T cell lymphoma (CTCL) (type B LyP cells) (Willemze et al., 1982). In most cases the large atypical cells have an activated helper T cell phenotype (CD30+, CD4+) (Kadin et al., 1985). Approximately 10–20% of LyP cases are associated with a malignant lymphoma, usually CTCL, HD, or a CD30+ large cell anaplastic lymphoma (ALCL), (Weinman and Ackerman, 1981; Willemze et al., 1982; Sanchez et al., 1983; Wantzin et al., 1985; Harrington et al., 1989; Kaudewitz et al., 1990). The skin lesions of LyP can precede, coexist with, or follow the associated lymphoma (Ibid).
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Kadin, M.E., Davis, T.H., Balk, S.P., Newcom, S.R., Cheifitz, S., Massague, J. (1994). Mechanism for Tumor Progression in Lymphomatoid Papulosis: Hypothesis Based on Studies of Tumor Cell Lines Clonally Derived from Lymphomatoid Papulosis. In: Lambert, W.C., Giannotti, B., van Vloten, W.A. (eds) Basic Mechanisms of Physiologic and Aberrant Lymphoproliferation in the Skin. NATO ASI Series, vol 265. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1861-7_35
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