Oncogenic Drivers of Breast Implant-Associated Anaplastic Large Cell Lymphoma.
Oncogenic Drivers of Breast Implant-Associated Anaplastic Large Cell Lymphoma.
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乳房植入相关的间变性大细胞淋巴瘤的致癌驱动因素。
DOI：
10.1097/prs.0000000000006331
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发表时间：
2020
影响因子：
3.6
通讯作者：
Vasconez,HenryC
中科院分区：
文献类型：
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作者：
DeCoster,RyanC;Rinker,BrianD;Butterfield,TimothyA;Vasconez,HenryC
我们非常高兴地阅读了Blombery等人的文章“乳腺植入物相关间变性大细胞淋巴瘤的分子驱动因素”。1出现在整形和重建外科乳腺植入物相关间变性大细胞淋巴瘤（BIA-ALCL）增刊中，2该文章简要回顾了当前围绕这种罕见恶性肿瘤发病机制的分子机制的文献。作者在这一重要领域继续开展工作，值得赞扬。我们特别感兴趣的是作者关注疾病的遗传驱动因素和JAK/STAT 3通路在BIA-ALCL发病机制中的作用。在过去的二十年里，由于世界各地实验室的重要工作，对BIA-ALCL的理解发生了巨大的变化，这些工作继续推动了对该疾病的认识。尽管有这些努力，阐明BIA-ALCL肿瘤发生和进展的分子机制仍然是一个挑战。缺乏动物模型限制了假设检验，仍然是该领域进展的障碍。虽然肿瘤细胞系提供了早期洞察致病性，苛刻的生长要求和异种移植的困难导致他们的中止。因此，临床标本已成为研究BIA-ALCL发病机制的宝贵而有限的资源，许多假说试图解释BIA-ALCL的发病机制。3尽管有限的科学证据阻碍了统一理论的发展，4但已经假设了刺激事件，如乳房袋的重复性创伤、巨噬细胞吞噬颗粒物质（例如，植入体中的硅胶）、细菌接种、病毒病原体和过敏原驱动的原因。结合这些假设中的一个或多个，异常基因表达也被认为在BIA-ALCL从慢性炎症状态发展为完全恶性肿瘤的致癌转化中发挥关键作用。
It is with great pleasure that we read the article “Molecular Drivers of Breast Implant-Associated Anaplastic Large Cell Lymphoma” by Blombery et al. 1 Appearing in the Plastic and Reconstructive Surgery breast implantassociated anaplastic large cell lymphoma (BIA-ALCL) supplement, 2 the article concisely reviews the current literature surrounding the molecular mechanisms implicated in the pathogenesis of this rare malignancy. The authors are to be commended for their continued work in this important area. Of particular interest to us was the authors’ focus on the genetic drivers of the disease and the role of the JAK/STAT3 pathway in the pathogenesis of BIA-ALCL. The understanding of BIA-ALCL has evolved immensely over the past two decades as a result of significant works from laboratories around the world that have continued to push knowledge of the disease forward. Despite these efforts, elucidating the molecular mechanisms responsible for BIA-ALCL tumorigenesis and progression remains a challenge. The lack of an animal model has limited hypothesis testing and remains a barrier to progress in the field. Although tumor cell lines provided early insight into pathogenicity, demanding growth requirements and difficulties with heterotransplantation led to their discontinuation. As a result, clinical specimens have become an invaluable but finite resource for mechanistic investigations of the disease.A number of hypotheses attempting to explain the pathogenesis of BIA-ALCL have been put forth. 3 Although limited scientific evidence has precluded development of a unifying theory, 4 inciting events such as repetitive trauma to the breast pocket, macrophage phagocytosis of particulate matter (eg, silicone from the implant), bacterial inoculation, viral pathogens, and an allergen-driven cause have been postulated. In combination with one or more of these postulates, aberrant gene expression is also thought to play a critical role in the oncogenic transformation of BIA-ALCL as it progresses from a chronic inflammatory state to a full-blown malignancy.