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Primary cutaneous CD30(+) anaplastic large cell lymphoma associated with fingolimod.

fingolimod, a disease-modifying treatment licenced (FDA approved in 2010) for relapsing-remitting multiple sclerosis (RRMS), is a modulator for four of the five known sphingosine-1-phosphate (S1P) receptor subtypes widely expressed in tissues including endothelial cells, lymphocytes, smooth muscle and neural cells (1). S1P receptor type 1 (S1PR1) is predominantly expressed by lymphocytes and represents the key molecular target for the therapeutic effect of fingolimod in multiple sclerosis (MS), by acting as a functional antagonist of the S1P receptor causing inhibition of lymphocyte egress from lymph nodes. This prevents the migration of lymphocytes into the peripheral tissues including the central nervous system (CNS) which reduces the expression of pro-inflammatory cytokines involved in the pathogenesis of MS. This article is protected by copyright. All rights reserved.

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