Gram-Negative Bacterial Lipopolysaccharide Promotes Tumor Cell Proliferation in Breast Implant-Associated Anaplastic Large-Cell Lymphoma
Breast implant-associated anaplastic large-cell lymphoma (BIA-ALCL) is a distinct malignancy associated with textured breast implants. We investigated whether bacteria could trigger the activation and multiplication of BIA-ALCL cells in vitro. BIA-ALCL patient-derived BIA-ALCL tumor cells, BIA-ALCL...
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MDPI AG
2021
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oai:doaj.org-article:e2f79716593c4317a03ff18b5949a9e22021-11-11T15:27:41ZGram-Negative Bacterial Lipopolysaccharide Promotes Tumor Cell Proliferation in Breast Implant-Associated Anaplastic Large-Cell Lymphoma10.3390/cancers132152982072-6694https://doaj.org/article/e2f79716593c4317a03ff18b5949a9e22021-10-01T00:00:00Zhttps://www.mdpi.com/2072-6694/13/21/5298https://doaj.org/toc/2072-6694Breast implant-associated anaplastic large-cell lymphoma (BIA-ALCL) is a distinct malignancy associated with textured breast implants. We investigated whether bacteria could trigger the activation and multiplication of BIA-ALCL cells in vitro. BIA-ALCL patient-derived BIA-ALCL tumor cells, BIA-ALCL cell lines, cutaneous ALCL cell lines, an immortal T-cell line (MT-4), and peripheral blood mononuclear cells (PBMC) from BIA-ALCL, capsular contracture, and primary augmentation patients were studied. Cells were subjected to various mitogenic stimulation assays including plant phytohemagglutinin (PHA), Gram-negative bacterial lipopolysaccharide (LPS), Staphylococcal superantigens enterotoxin A (SEA), toxic shock syndrome toxin-1 (TSST-1), or sterilized implant shells. Patient-derived BIA-ALCL tumor cells and BIA-ALCL cell lines showed a unique response to LPS stimulation. This response was dampened significantly in the presence of a Toll-like receptor 4 (TLR4) inhibitor peptide. In contrast, cutaneous ALCL cells, MT-4, and PBMC cells from all patients responded significantly more to PHA, SEA, and TSST-1 than to LPS. Breast implant shells of all surface grades alone did not produce a proliferative response of BIA-ALCL cells, indicating the breast implant does not act as a pro-inflammatory stimulant. These findings indicate a possible novel pathway for LPS to promote BIA-ALCL cell proliferation via a TLR4 receptor-mediated bacterial transformation of T-cells into malignancy.Maria MempinHonghua HuKaren VickeryMarshall E. KadinH. Miles PrinceNicola KouttabJohn W. MorganWilliam P. AdamsAnand K. DevaMDPI AGarticlebreast implant-associated anaplastic large-cell lymphomalipopolysaccharidetumor cellproliferationT-cells’ malignancyNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENCancers, Vol 13, Iss 5298, p 5298 (2021) |
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breast implant-associated anaplastic large-cell lymphoma lipopolysaccharide tumor cell proliferation T-cells’ malignancy Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 |
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breast implant-associated anaplastic large-cell lymphoma lipopolysaccharide tumor cell proliferation T-cells’ malignancy Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Maria Mempin Honghua Hu Karen Vickery Marshall E. Kadin H. Miles Prince Nicola Kouttab John W. Morgan William P. Adams Anand K. Deva Gram-Negative Bacterial Lipopolysaccharide Promotes Tumor Cell Proliferation in Breast Implant-Associated Anaplastic Large-Cell Lymphoma |
description |
Breast implant-associated anaplastic large-cell lymphoma (BIA-ALCL) is a distinct malignancy associated with textured breast implants. We investigated whether bacteria could trigger the activation and multiplication of BIA-ALCL cells in vitro. BIA-ALCL patient-derived BIA-ALCL tumor cells, BIA-ALCL cell lines, cutaneous ALCL cell lines, an immortal T-cell line (MT-4), and peripheral blood mononuclear cells (PBMC) from BIA-ALCL, capsular contracture, and primary augmentation patients were studied. Cells were subjected to various mitogenic stimulation assays including plant phytohemagglutinin (PHA), Gram-negative bacterial lipopolysaccharide (LPS), Staphylococcal superantigens enterotoxin A (SEA), toxic shock syndrome toxin-1 (TSST-1), or sterilized implant shells. Patient-derived BIA-ALCL tumor cells and BIA-ALCL cell lines showed a unique response to LPS stimulation. This response was dampened significantly in the presence of a Toll-like receptor 4 (TLR4) inhibitor peptide. In contrast, cutaneous ALCL cells, MT-4, and PBMC cells from all patients responded significantly more to PHA, SEA, and TSST-1 than to LPS. Breast implant shells of all surface grades alone did not produce a proliferative response of BIA-ALCL cells, indicating the breast implant does not act as a pro-inflammatory stimulant. These findings indicate a possible novel pathway for LPS to promote BIA-ALCL cell proliferation via a TLR4 receptor-mediated bacterial transformation of T-cells into malignancy. |
format |
article |
author |
Maria Mempin Honghua Hu Karen Vickery Marshall E. Kadin H. Miles Prince Nicola Kouttab John W. Morgan William P. Adams Anand K. Deva |
author_facet |
Maria Mempin Honghua Hu Karen Vickery Marshall E. Kadin H. Miles Prince Nicola Kouttab John W. Morgan William P. Adams Anand K. Deva |
author_sort |
Maria Mempin |
title |
Gram-Negative Bacterial Lipopolysaccharide Promotes Tumor Cell Proliferation in Breast Implant-Associated Anaplastic Large-Cell Lymphoma |
title_short |
Gram-Negative Bacterial Lipopolysaccharide Promotes Tumor Cell Proliferation in Breast Implant-Associated Anaplastic Large-Cell Lymphoma |
title_full |
Gram-Negative Bacterial Lipopolysaccharide Promotes Tumor Cell Proliferation in Breast Implant-Associated Anaplastic Large-Cell Lymphoma |
title_fullStr |
Gram-Negative Bacterial Lipopolysaccharide Promotes Tumor Cell Proliferation in Breast Implant-Associated Anaplastic Large-Cell Lymphoma |
title_full_unstemmed |
Gram-Negative Bacterial Lipopolysaccharide Promotes Tumor Cell Proliferation in Breast Implant-Associated Anaplastic Large-Cell Lymphoma |
title_sort |
gram-negative bacterial lipopolysaccharide promotes tumor cell proliferation in breast implant-associated anaplastic large-cell lymphoma |
publisher |
MDPI AG |
publishDate |
2021 |
url |
https://doaj.org/article/e2f79716593c4317a03ff18b5949a9e2 |
work_keys_str_mv |
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