Etiology of Breast Implant-Associated Anaplastic Large Cell Lymphoma (BIA-ALCL): Current Directions in Research

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14740%2F20%3A00118309" target="_blank" >RIV/00216224:14740/20:00118309 - isvavai.cz</a>

Result on the web

<a href="https://www.mdpi.com/2072-6694/12/12/3861" target="_blank" >https://www.mdpi.com/2072-6694/12/12/3861</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3390/cancers12123861" target="_blank" >10.3390/cancers12123861</a>

Result language

angličtina

Original language name

Etiology of Breast Implant-Associated Anaplastic Large Cell Lymphoma (BIA-ALCL): Current Directions in Research

Original language description

Simple Summary The first report of breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) was in 1997. Although BIA-ALCL develops around breast implants, it is considered a cancer of the immune system and not a cancer of the breast ducts or lobules. Nearly all confirmed cases to date have been associated with textured surface (versus smooth surface) breast implants. As physicians have become more aware of BIA-ALCL, so has the number of reported cases, although the number of cases remains low. In most instances, patients have an excellent prognosis following removal of the breast implant and its surrounding fibrous capsule. Many theories on factors that trigger the development of BIA-ALCL, such as the presence of bacteria, have been proposed. However, the sequence(s) of events that follow the initial triggering event(s) have not been fully determined. This article summarizes the current scientific knowledge on the development of BIA-ALCL. 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.

Czech name

—

Czech description

—

Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30204 - Oncology

Project

—

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2020

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Cancers

ISSN

2072-6694

e-ISSN

—

Volume of the periodical

12

Issue of the periodical within the volume

12

Country of publishing house

CH - SWITZERLAND

Number of pages

14

Pages from-to

3861

UT code for WoS article

000601744600001

EID of the result in the Scopus database

2-s2.0-85098283166