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      Differential expression of estrogen receptor–α on follicular dendritic cells from patients with grade 1‐2 and grade 3 follicular lymphoma

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          Abstract

          Hormone therapy has been used for patients with estrogen receptor alpha (ERα)–positive breast cancers. Recently, some studies reported the expression of ERα on neoplastic cells from B‐cell lymphomas. However, there has been only one report of ERα expression on the follicular dendritic cells (FDCs) that structurally and functionally support the microenvironment of follicular lymphomas (FLs). The objective of this study was to investigate the frequency of ERα expression on FDCs in nonneoplastic reactive lymphoid tissues and to compare the frequency of ERα expression on FDCs in the axillary lymph nodes between patients with and without antiestrogen therapy and among patients with grades 1‐3 of FL. Reverse transcription–polymerase chain reaction was performed to detect ERα mRNA in FL. In nonneoplastic germinal centers (GCs) from patients with tonsillitis or reactive lymphadenitis, ERα was expressed in the light zone. ERα‐positive cells strongly correlated with the width of GCs ( r s = 0.81, P < 0.01) and the CD21‐positive ( r s = 0.69, P < 0.01) and CD23‐positive ( r s = 0.83, P < 0.01) FDC meshwork. The axillary lymph nodes had fewer ERα‐positive cells, smaller GCs, and a looser CD21‐ and CD23‐positive FDC meshwork with hormone therapy than without hormone therapy ( P < 0.01). Neoplastic follicles of G1‐2 FL had more ERα‐positive cells and a larger CD23 + FDC meshwork than those of G3 FL ( P < 0.01). ERα mRNA was detected in both G1‐2 FL and G3 FL by reverse transcription–polymerase chain reaction. In conclusion, these results suggested that antiestrogen hormone therapy may decrease the number of ERα‐positive FDCs and that the responses mediated by the estrogen‐ERα interaction on FDCs may differ between G1‐2 FL and G3 FL.

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          NIH Image to ImageJ: 25 years of image analysis.

          For the past 25 years NIH Image and ImageJ software have been pioneers as open tools for the analysis of scientific images. We discuss the origins, challenges and solutions of these two programs, and how their history can serve to advise and inform other software projects.
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            The tumour microenvironment influences survival and time to transformation in follicular lymphoma in the rituximab era

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              A rare fraction of drug-resistant follicular lymphoma cancer stem cells interacts with follicular dendritic cells to maintain tumourigenic potential.

              Follicular lymphoma (FL) comprises nearly 25% of non-Hodgkin lymphoma cases and is clinically characterized by initial sensitivity to chemotherapy followed by relapse. FL stroma contains a special type of stromal cell found in the germinal centre of lymph nodes-the follicular dendritic cell (FDC). We first isolated tumourigenic cells from the FL cell line FLK-1 by side population (SP) technique, and found that SP cells, which express ABCG2, were enriched by chemotherapy and radiation treatments. In vitro, SP cells were attracted by and adhered to FDCs through chemokine (C-X-C motif) ligand 12/chemokine (C-X-C motif) receptor 4 (CXCL12/CXCR4) signalling. In vivo, limiting dilution assays showed SP cells were highly enriched in cancer stem cells (CSC), but required FDC for tumour formation in non-obese diabetic/severe combined immunodeficiency mice. Treatment with AMD3100, a specific CXCL12/CXCR4 inhibitor, eliminated tumour growth. These findings were then verified with FL cells isolated from an FL patient's ascitic fluid (FLA-1). Finally, we detected the ABCG2 expressing lymphoma cells in FL clinical specimens. Thus, we found that the highly tumourigenic FL cells having CSC-like activities (FL-SC) interact with FDCs in a CXCL12/CXCR4 dependent manner to resist chemotherapy. Our results indicate the importance of FL-SC and niche cell signalling in maintaining tumourigenicity. These signals represent novel targets for CSC eradication. © 2012 Blackwell Publishing Ltd.
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                Author and article information

                Contributors
                r-ooe@med.id.yamagata-u.ac.jp
                Journal
                Hematol Oncol
                Hematol Oncol
                10.1002/(ISSN)1099-1069
                HON
                Hematological Oncology
                John Wiley and Sons Inc. (Hoboken )
                0278-0232
                1099-1069
                20 March 2019
                April 2019
                : 37
                : 2 ( doiID: 10.1002/hon.v37.2 )
                : 151-159
                Affiliations
                [ 1 ] Department of Pathological Diagnostics Yamagata University Faculty of Medicine Yamagata Japan
                [ 2 ] Department of Pathology Harbin Medical University Cancer Hospital Harbin China
                [ 3 ] Department of Neurology, Hematology, Metabolism, Endocrinology and Diabetology Yamagata University Faculty of Medicine Yamagata Japan
                [ 4 ] Department of Surgery Yonezawa City Hospital Yonezawa Japan
                [ 5 ] Department of Gastroenterological, General, Breast and Thyroid Surgery Yamagata University Faculty of Medicine Yamagata Japan
                Author notes
                [*] [* ] Correspondence

                Rintaro Ohe, Department of Pathological Diagnostics, Yamagata University Faculty of Medicine, 2‐2‐2 Iida‐Nishi, Yamagata 990‐9585, Japan.

                Email: r-ooe@ 123456med.id.yamagata-u.ac.jp

                Author information
                https://orcid.org/0000-0002-8035-791X
                Article
                HON2577 HON-19-0007.R1
                10.1002/hon.2577
                6593816
                30736096
                db4337a0-80ca-44b6-bebd-0472fb435817
                © 2019 The Authors Hematological Oncology Published by John Wiley & Sons Ltd

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 08 January 2019
                : 27 January 2019
                : 05 February 2019
                Page count
                Figures: 5, Tables: 1, Pages: 9, Words: 3462
                Funding
                Funded by: Japan Society for the Promotion of Science
                Award ID: JP17K08736
                Categories
                Original Research Article
                Original Research Articles
                Custom metadata
                2.0
                hon2577
                April 2019
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.5 mode:remove_FC converted:26.06.2019

                cd23,estrogen receptor alpha,follicular dendritic cell,follicular lymphoma

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