Does Breast Implant-Associated ALCL Begin as a Lymphoproliferative Disorder?

TitleDoes Breast Implant-Associated ALCL Begin as a Lymphoproliferative Disorder?
Publication TypeJournal Article
Year of Publication2020
AuthorsKadin ME, Adams WP, Inghirami G, Di Napoli A
JournalPlast Reconstr Surg
Date Published2020 01
KeywordsBiopsy, Breast, Breast Implantation, Breast Implants, Breast Neoplasms, Female, Humans, Lymphoma, Large-Cell, Anaplastic

Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) has been included as a provisional entity in the revised version of the World Health Organization Classification of Tumors of Haematopoietic and Lymphoid Tissue. To increase opportunities to intervene with early diagnosis, treatment, and possible prevention, it is important to consider that BIA-ALCL may evolve from a preexisting lymphoproliferative disorder characterized by (1) an indolent localized (in situ) disease in approximately 80 percent of reported cases; (2) a requirement for external cytokine stimulation for cell survival; (3) CD30 cells in some clinically benign seromas/capsules; (4) undetected T-cell clonality in some cases; (5) JAK/STAT mutations in only a minority of cases; and (6) cure by capsulectomy and implant removal in most cases. BIA-ALCL resembles CD30 cutaneous lymphoproliferative disorder: ALK, CD30 anaplastic cells with an aberrant T-cell phenotype; overexpression of oncogenes (JUNB, SATB1, pSTAT3, SOCS3) in lymphomatoid papulosis; frequent apoptosis; complete spontaneous regression in lymphomatoid papulosis; and partial spontaneous regression in cutaneous ALCL. Unlike CD30 cutaneous lymphoproliferative disorder, BIA-ALCL cannot be readily observed over time to study the different steps in progression to ALCL. BIA-ALCL also shares features of lymphomas of mucosa-associated lymphoid tissue, which are clinically indolent, initially localized, antigen driven, and caused by Gram-negative bacteria. Further studies of cytokines, clonality, mutations, and other biomarkers are needed to identify possible premalignant steps in the evolution of benign late seromas to BIA-ALCL.

Alternate JournalPlast Reconstr Surg
PubMed ID31577659
Related Faculty: 
Giorgio Inghirami, M.D.

Pathology & Laboratory Medicine 1300 York Avenue New York, NY 10065 Phone: (212) 746-6464
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