Format

Send to

Choose Destination
Aesthet Surg J. 2019 Jan 31;39(Supplement_1):S21-S27. doi: 10.1093/asj/sjy229.

The Cellular Origins of Breast Implant-Associated Anaplastic Large Cell Lymphoma (BIA-ALCL): Implications for Immunogenesis.

Author information

1
Division of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Cambridge, UK.

Abstract

The exact cellular origins of most malignancies are unknown, largely because of the complex nature of malignancies, and because the potential vast number of pathways towards transformation are difficult to discern from established growths. This is compounded by the fact that cancer cells have evolved rather than being the consequence of a design process, with most data collected from (sometimes epidemiological) studies of large numbers of related malignancies. In the case of breast implant-associated anaplastic large cell lymphoma (BIA-ALCL), the relative rarity of this disease, coupled with limited insight into its biological basis, have hampered progress. The known facts that are holding up as our knowledge increases with rising incidences are that most cases have been reported in the context of textured breast implants, although not all women with these implants develop BIA-ALCL, and cure for early-stage disease (accounting for the majority of patients) can be achieved via complete capsulectomy and implant removal. However, some theories can be gleaned from the limited biological studies conducted to date whereby a T-helper cell derivation is implicated, with its specific and apparent subset of origin dependent on, and shaped by, a number of factors, including the inflammatory microenvironment (the presence of other inflammatory cell types), the driving antigen (bacterial and/or synthetic), the acquisition of driving oncogenic events, and the inherent genetics/health status of the patient.

PMID:
30715172
PMCID:
PMC6355097
[Available on 2020-01-31]
DOI:
10.1093/asj/sjy229

Supplemental Content

Full text links

Icon for Silverchair Information Systems
Loading ...
Support Center