{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T22:01:21Z","timestamp":1761948081115},"reference-count":26,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2015,6,24]],"date-time":"2015-06-24T00:00:00Z","timestamp":1435104000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Br J Haematol"],"published-print":{"date-parts":[[2015,9]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>To obtain further insights into the biological differences of anaplastic lymphoma kinase positive anaplastic large cell lymphoma (<jats:styled-content style=\"fixed-case\">ALK<\/jats:styled-content>+ <jats:styled-content style=\"fixed-case\">ALCL<\/jats:styled-content>) and classical Hodgkin lymphoma (<jats:styled-content style=\"fixed-case\">HL<\/jats:styled-content>), we screened microbial culture filtrates to search for compounds that would exert a significantly greater effect on the viability of <jats:styled-content style=\"fixed-case\">ALK<\/jats:styled-content>+ <jats:styled-content style=\"fixed-case\">ALCL<\/jats:styled-content> cell lines compared to <jats:styled-content style=\"fixed-case\">HL<\/jats:styled-content> cell lines and identified Brefeldin A (<jats:styled-content style=\"fixed-case\">BFA<\/jats:styled-content>) as a suitable candidate. <jats:styled-content style=\"fixed-case\">BFA<\/jats:styled-content> inhibited phosphorylation of <jats:styled-content style=\"fixed-case\">ALK<\/jats:styled-content> and its downstream molecule, signal transducer and activator of transcription 3 (<jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>3), one of the central pathways for the survival of <jats:styled-content style=\"fixed-case\">ALK<\/jats:styled-content>+ <jats:styled-content style=\"fixed-case\">ALCL<\/jats:styled-content> cells. In <jats:styled-content style=\"fixed-case\">HL<\/jats:styled-content> cell lines <jats:styled-content style=\"fixed-case\">BFA<\/jats:styled-content> did not affect <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>30 expression or\u00a0constitutive nuclear factor (<jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>)\u2010\u03baB activity, both of which are critical for\u00a0<jats:styled-content style=\"fixed-case\">HL<\/jats:styled-content> cell survival. <jats:styled-content style=\"fixed-case\">BFA<\/jats:styled-content> induced disruption of the Golgi apparatus in <jats:styled-content style=\"fixed-case\">ALK<\/jats:styled-content>+ <jats:styled-content style=\"fixed-case\">ALCL<\/jats:styled-content> cell lines, which was accompanied by a decrease in active <jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content>\u2010ribosylation factor 1 (<jats:styled-content style=\"fixed-case\">ARF<\/jats:styled-content>1), whereas <jats:styled-content style=\"fixed-case\">BFA<\/jats:styled-content> had no significant effect on these parameters in <jats:styled-content style=\"fixed-case\">HL<\/jats:styled-content> cell lines. These results add extra insights into the biological distinction between <jats:styled-content style=\"fixed-case\">ALK<\/jats:styled-content>+ <jats:styled-content style=\"fixed-case\">ALCL<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">HL<\/jats:styled-content> cells and highlight the Golgi apparatus as a target for the treatment of <jats:styled-content style=\"fixed-case\">ALK<\/jats:styled-content>+ <jats:styled-content style=\"fixed-case\">ALCL<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/bjh.13508","type":"journal-article","created":{"date-parts":[[2015,6,24]],"date-time":"2015-06-24T08:41:08Z","timestamp":1435135268000},"page":"837-846","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Brefeldin A exerts differential effects on anaplastic lymphoma kinase positive anaplastic large cell lymphoma and classical Hodgkin lymphoma cell lines"],"prefix":"10.1111","volume":"170","author":[{"given":"Takashi","family":"Toda","sequence":"first","affiliation":[{"name":"Department of Applied Chemistry Faculty of Science and Technology Keio University Kanagawa Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mariko","family":"Watanabe","sequence":"additional","affiliation":[{"name":"Department of Haematology School of Medicine Kitasato University Kanagawa Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Junji","family":"Kawato","sequence":"additional","affiliation":[{"name":"Department of Applied Chemistry Faculty of Science and Technology Keio University Kanagawa Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marshall E.","family":"Kadin","sequence":"additional","affiliation":[{"name":"Boston University School of Medicine and Department of Dermatology and Skin Surgery Roger Williams Medical Center Providence RI USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masaaki","family":"Higashihara","sequence":"additional","affiliation":[{"name":"Department of Haematology School of Medicine Kitasato University Kanagawa Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takao","family":"Kunisada","sequence":"additional","affiliation":[{"name":"Bioscience Institute Meiji Seika Pharma Co. 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