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  Age-Related Gliosis Promotes Central Nervous System Lymphoma through CCL19-Mediated Tumor Cell Retention

O'Connor, T., Zhou, X., Kosla, J., Adili, A., Beccaria, M. G., Kotsiliti, E., et al. (2019). Age-Related Gliosis Promotes Central Nervous System Lymphoma through CCL19-Mediated Tumor Cell Retention. CANCER CELL, 36(3), 250-267.e9. doi:10.1016/j.ccell.2019.08.001.

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 Creators:
O'Connor, Tracy1, Author
Zhou, Xiaolan1, Author
Kosla, Jan1, Author
Adili, Arlind1, Author
Beccaria, Maria Garcia1, Author
Kotsiliti, Elena1, Author
Pfister, Dominik1, Author
Johlke, Anna-Lena1, Author
Sinha, Ankit2, Author           
Sankowski, Roman1, Author
Schick, Markus1, Author
Lewis, Richard1, Author
Dokalis, Nikolaos1, Author
Seubert, Bastian1, Author
Hoechst, Bastian1, Author
Inverso, Donato1, Author
Heide, Danijela1, Author
Zhang, Wenlong1, Author
Weihrich, Petra1, Author
Manske, Katrin1, Author
Wohlleber, Dirk1, AuthorAnton, Martina1, AuthorHoellein, Alexander1, AuthorSeleznik, Gitta1, AuthorBremer, Juliane1, AuthorBleul, Sabine1, AuthorAugustin, Helmut G.1, AuthorScherer, Florian1, AuthorKoedel, Uwe1, AuthorWeber, Achim1, AuthorProtzer, Ulrike1, AuthorFoerster, Reinhold1, AuthorWirth, Thomas1, AuthorAguzzi, Adriano1, AuthorMeissner, Felix2, Author           Prinz, Marco1, AuthorBaumann, Bernd1, AuthorHoepken, Uta E.1, AuthorKnolle, Percy A.1, Authorvon Baumgarten, Louisa1, AuthorKeller, Ulrich1, AuthorHeikenwalder, Mathias1, Author more..
Affiliations:
1external, ou_persistent22              
2Meissner, Felix / Experimental Systems Immunology, Max Planck Institute of Biochemistry, Max Planck Society, ou_2149678              

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Free keywords: PRIMARY CNS LYMPHOMA; IMMUNOPHENOTYPE MIGHT; BURKITT-LYMPHOMA; POOR-PROGNOSIS; WEB TOOL; ACTIVATION; NEUROINFLAMMATION; AUTOIMMUNE; EXPRESSION; IBRUTINIBOncology; Cell Biology;
 Abstract: How lymphoma cells (LCs) invade the brain during the development of central nervous system lymphoma (CNSL) is unclear. We found that NF-KB-induced gliosis promotes CNSL in immunocompetent mice. Gliosis elevated cell-adhesion molecules, which increased LCs in the brain but was insufficient to induce CNSL. Astrocyte-derived CCL19 was required for gliosis-induced CNSL. Deleting CCL19 in mice or CCR7 from LCs abrogated CNSL development. Two-photon microscopy revealed LCs transiently entering normal brain parenchyma. Astrocytic CCL19 enhanced parenchymal CNS retention of LCs, thereby promoting CNSL formation. Aged, gliotic wild-type mice were more susceptible to forming CNSL than young wild-type mice, and astrocytic CCL19 was observed in both human gliosis and CNSL. Therefore, CCL19-CCR7 interactions may underlie an increased age-related risk for CNSL.

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Language(s): eng - English
 Dates: 2019
 Publication Status: Published in print
 Pages: 27
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Degree: -

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Title: CANCER CELL
Source Genre: Journal
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Publ. Info: 50 HAMPSHIRE ST, FLOOR 5, CAMBRIDGE, MA 02139 USA : CELL PRESS
Pages: - Volume / Issue: 36 (3) Sequence Number: - Start / End Page: 250 - 267.e9 Identifier: ISSN: 1535-6108