LYMPHOMA: Edited by Dominique BronNew insights into breast implant-associated anaplastic large cell lymphomaLaurent, Camillea,b,∗; Haioun, Corinnec,d; Brousset, Pierrea,b; Gaulard, Philipped,e,∗Author Information aDépartement de Pathologie, Institut Universitaire du Cancer de Toulouse, CHU de Toulouse bLaboratoire d’excellence Toucan, INSERM U.1037, Centre de Recherche en Cancérologie de Toulouse-Purpan, Toulouse cUnité Hémopathies Lymphoides, Groupe Hospitalier Henri Mondor dINSERM U955, Université Paris-Est eDépartement de Pathologie, Groupe Hospitalier Henri Mondor, Créteil, France Correspondence to Camille Laurent, Laboratoire d’Anatomie et de Cytologie Pathologique, CHU, IUCT Oncopole, 1 avenue Irène Joliot-Curie, 31059 Toulouse; Université Paul-Sabatier, Toulouse F-31400, France. Tel: +33531156199; fax: +33531156594; e-mail: [email protected] Current Opinion in Oncology: September 2018 - Volume 30 - Issue 5 - p 292-300 doi: 10.1097/CCO.0000000000000476 Buy Metrics Abstract Purpose of review Breast implant-associated anaplastic large cell lymphoma (BI-ALCL) is a rare form of lymphoma arising adjacent to a breast implant. We aim to review the pathogenesis and clinico-biological features of BI-ALCL. Recent findings BI-ALCL is a new provisional entity in the 2017 updated WHO classification. Among several hypotheses, BI-ALCL development seems to be determined by the interaction of immune response related to implant products and additional genetic events. Summary BI-ALCL is an uncommon T-cell lymphoma which is increasingly diagnosed since its first description in 1997 with 500 estimated cases worldwide. Two BI-ALCL subtypes correlating with clinical presentation have been described. Although most BI-ALCL patients with tumor cell proliferation restricted to the periprosthetic effusion and capsule have excellent outcomes, other patients presenting with a tumor mass, may have a more aggressive disease. The pathogenesis of BI-ALCL remains elusive. It is postulated that local chronic inflammation elicitated by bacterial infection or implant products may promote the activation and proliferation of T cells. Additional genetic events resulting in the activation JAK/STAT pathway are also incriminated. Further investigations are needed to better characterize the pathogenesis of this disease in order to determine the potential risk to develop BI-ALCL after surgical implants. Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.