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Alterations in the Rho pathway contribute to Epstein-Barr virus-induced lymphomagenesis in immunosuppressed environments

Authors
Cho, SY | Sung, CO | Chae, J | Lee, J | Na, D | Kang, W | Kang, J | Min, S | Lee, A | Kwak, E | Kim, J | Choi, B | Kim, H | Chuang, JH | Pak, HK | Park, CS | Park, S | Ko, YH | Lee, D  | Roh, J | Cho, MS | Park, S | Ju, YS | Suh, YS | Kong, SH | Lee, HJ | Keck, J | Banchereau, J | Liu, ET | Kim, WH | Park, H | Yang, HK | Kim, JI | Lee, C
Citation
Blood, 131(17). : 1931-1941, 2018
Journal Title
Blood
ISSN
0006-49711528-0020
Abstract
Epstein-Barr virus (EBV)-positive diffuse large B-cell lymphomas (EBV(+)-DLBLs) tend to occur in immunocompromised patients, such as the elderly or those undergoing solid organ transplantation. The pathogenesis and genomic characteristics of EBV(+)-DLBLs are largely unknown because of the limited availability of human samples and lack of experimental animal models. We observed the development of 25 human EBV(+)-DLBLs during the engraftment of gastric adenocarcinomas into immunodeficient mice. An integrated genomic analysis of the human-derived EBV(+)-DLBLs revealed enrichment of mutations in Rho pathway genes, including RHPN2, and Rho pathway transcriptomic activation. Targeting the Rho pathway using a Rho-associated protein kinase (ROCK) inhibitor, fasudil, markedly decreased tumor growth in EBV(+)-DLBL patient-derived xenograft (PDX) models. Thus, alterations in the Rho pathway appear to contribute to EBV-induced lymphomagenesis in immunosuppressed environments.
MeSH

DOI
10.1182/blood-2017-07-797209
PMID
29475961
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Journal Papers > School of Medicine / Graduate School of Medicine > Pathology
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