Somatic IL4R mutations in primary mediastinal large B-cell lymphoma lead to constitutive JAK-STAT signaling activation
Elena Viganò(BC Cancer Agency), Jay Gunawardana(BC Cancer Agency), Anja Mottok(BC Cancer Agency), Tessa Van Tol(BC Cancer Agency), Katina Mak(BC Cancer Agency), Fong Chun Chan(BC Cancer Agency), Lauren C. Chong(BC Cancer Agency), Elizabeth A. Chavez(BC Cancer Agency), Bruce W. Woolcock(BC Cancer Agency), Katsuyoshi Takata(BC Cancer Agency), David D. W. Twa(BC Cancer Agency), Hennady P. Shulha(BC Cancer Agency), Adèle Telenius(BC Cancer Agency), Olga A. Kutovaya(BC Cancer Agency), Stacy Hung(BC Cancer Agency), Shannon Healy(BC Cancer Agency), Susana Ben‐Neriah(BC Cancer Agency), Karen Leroy(Délégation Paris 5), Philippe Gaulard(Inserm), Arjan Diepstra(University Medical Center Groningen), Robert Kridel(BC Cancer Agency), Kerry J. Savage(BC Cancer Agency), Lisa M. Rimsza(University of Arizona), Randy D. Gascoyne(BC Cancer Agency), Christian Steidl(BC Cancer Agency)
Cited by 60Open Access
Abstract
Key Points Somatic IL4R mutations were identified in 24% of primary PMBCL cases (n = 62) and in 100% of PMBCL-derived cell lines. IL4R mutations lead to hyperphosphorylation of STAT proteins activating downstream immunoregulatory genes (CD23, CCL17).
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