Please use this identifier to cite or link to this item: http://hdl.handle.net/11434/1914
Title: Etiology of breast implant-associated anaplastic large cell lymphoma (BIA-ALCL): Current directions in research.
Authors: Prince, Miles
Other Authors: Deva, Anand
Turner, Suzanne
Kadin, Marshall
Magnusson, Mark
Miranda, Roberto
Inghirami, Giorgio
Adams, William
Keywords: Cancer
Neoplasms
Breast Implants
T-Cells
Antigens
Lymphoma
Breast Implant-Associated Anaplastic Large Cell Lymphoma
BIA-ALCL
Triggers
Cancer Services Clinical Institute, Epworth HealthCare, Victoria, Australia
Issue Date: Dec-2020
Publisher: MDPI
Citation: Cancers (Basel) . 2020 Dec 21;12(12):3861
Abstract: Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) is a CD30-positive, anaplastic lymphoma kinase-negative T-cell lymphoma. Where implant history is known, all confirmed cases to date have occurred in patients with exposure to textured implants. There is a spectrum of disease presentation, with the most common occurring as a seroma with an indolent course. A less common presentation occurs as locally advanced or, rarely, as metastatic disease. Here we review the immunological characteristics of BIA-ALCL and potential triggers leading to its development. BIA-ALCL occurs in an inflammatory microenvironment with significant lymphocyte and plasma cell infiltration and a prominent Th1/Th17 phenotype in advanced disease. Genetic lesions affecting the JAK/STAT signaling pathway are commonly present. Proposed triggers for the development of malignancy include mechanical friction, silicone implant shell particulates, silicone leachables, and bacteria. Of these, the bacterial hypothesis has received significant attention, supported by a plausible biologic model. In this model, bacteria form an adherent biofilm in the favorable environment of the textured implant surface, producing a bacterial load that elicits a chronic inflammatory response. Bacterial antigens, primarily of Gram-negative origin, may trigger innate immunity and induce T-cell proliferation with subsequent malignant transformation in genetically susceptible individuals. Although much remains to be elucidated regarding the multifactorial origins of BIA-ALCL, future research should focus on prevention and treatment strategies, recognizing susceptible populations, and whether decreasing the risk of BIA-ALCL is possible.
URI: http://hdl.handle.net/11434/1914
DOI: 10.3390/cancers12123861
PubMed URL: https://pubmed.ncbi.nlm.nih.gov/33371292/
ISSN: 2072-6694
Journal Title: Cancers
Type: Journal Article
Affiliated Organisations: Department of Plastic and Reconstructive Surgery, Macquarie University and the Integrated Specialist Healthcare Education and Research Foundation, Sydney, NSW 2109, Australia.
Division of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge CB2 1TN, UK.
Šárka Pospíšilová Research Group, CEITEC, Masaryk University, 601 77 Brno, Czech Republic.
Department of Dermatology, Roger Williams Medical Center, Providence, RI 02908, USA.
Boston University School of Medicine, Boston, MA 02908, USA.
Department of Plastic Surgery, School of Medicine, Griffith University, Southport, QLD 4222, Australia.
Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, VIC 3000, Australia.
Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Department of Pathology, Weill Cornell Medicine, New York, NY 10065, USA.
Department of Plastic Surgery, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Appears in Collections:Cancer Services

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