دورية أكاديمية
Cell of Origin and Immunologic Events in the Pathogenesis of Breast Implant-Associated Anaplastic Large-Cell Lymphoma.
| العنوان: | Cell of Origin and Immunologic Events in the Pathogenesis of Breast Implant-Associated Anaplastic Large-Cell Lymphoma. |
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| المؤلفون: | Turner, Suzanne D, Inghirami, Giorgio, Miranda, Roberto N, Kadin, Marshall E |
| بيانات النشر: | Elsevier BV //dx.doi.org/10.1016/j.ajpath.2019.09.005 Am J Pathol |
| سنة النشر: | 2020 |
| المجموعة: | Apollo - University of Cambridge Repository |
| مصطلحات موضوعية: | Breast Implants, Breast Neoplasms, Cell Lineage, Female, Humans, Lymphoma, Large-Cell, Anaplastic |
| الوصف: | Breast implant-associated anaplastic large-cell lymphoma (BIA-ALCL) is a CD30-positive, anaplastic lymphoma kinase-negative T-cell lymphoma. Nearly all cases have been associated with textured implants. Most cases are of effusion-limited, indolent disease, with an excellent prognosis after implant and capsule removal. However, capsular invasion and tumor mass have a more aggressive course and a fatal outcome risk. This review summarizes the current knowledge on BIA-ALCL cell of origin and immunologic factors underlying its pathogenesis. Cytokine expression profiling of BIA-ALCL cell lines and clinical specimens reveals a predominantly type 17 helper T-cell (Th17)/Th1 signature, implicating this as its cell of origin. However, a Th2 allergic inflammatory response is suggested by the presence of IL-13, with infiltration of eosinophils and IgE-coated mast cells in clinical specimens of BIA-ALCL. The microenvironment-induced T-cell plasticity, a factor increasingly appreciated, may partially explain these divergent results. Mutations resulting in constitutive Janus kinase (JAK)-STAT activation have been detected and associated with BIA-ALCL pathogenesis in a small number of cases. One possible scenario is that an inflammatory microenvironment stimulates an immune response, followed by polyclonal expansion of Th17/Th1 cell subsets with release of inflammatory cytokines and chemokines and accumulation of seroma. JAK-STAT3 gain-of-function mutations within this pathway and others may subsequently lead to monoclonal T-cell proliferation and clinical BIA-ALCL. Current research suggests that therapies targeting JAK proteins warrant investigation in BIA-ALCL. ; Writing and editorial assistance was provided to the authors by Robert Rydzewski, MS, CMPP, of Peloton Advantage, LLC, an OPEN Health company, Parsippany, NJ, and was funded by Allergan plc, Dublin, Ireland. |
| نوع الوثيقة: | article in journal/newspaper |
| وصف الملف: | Print-Electronic; application/pdf |
| اللغة: | English |
| العلاقة: | https://www.repository.cam.ac.uk/handle/1810/296971Test |
| DOI: | 10.17863/CAM.44012 |
| الإتاحة: | https://doi.org/10.17863/CAM.44012Test https://www.repository.cam.ac.uk/handle/1810/296971Test |
| حقوق: | Attribution-NonCommercial-NoDerivatives 4.0 International ; https://creativecommons.org/licenses/by-nc-nd/4.0Test/ |
| رقم الانضمام: | edsbas.F89CABF |
| قاعدة البيانات: | BASE |
| DOI: | 10.17863/CAM.44012 |
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