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INSIDE‐OUT VLA‐4 INTEGRIN ACTIVATION IS MAINTAINED IN IBRUTINIB‐TREATED CHRONIC LYMPHOCYTIC LEUKEMIA EXPRESSING CD49D: CLINICAL RELEVANCE
Author(s) -
Tissino E.,
Benedetti D.,
Herman S.E.,
Hacken E.,
Ahn I.E.,
Chaffee K.G.,
Bayer E.,
Haerzschel A.,
Gutjahr J.C.,
Postorino M.,
Santinelli E.,
Ayed A.,
Zaja F.,
Chiarenza A.,
Chigaev A.,
Sklar L.A.,
Burger J.A.,
Ferrajoli A.,
Shanafelt T.D.,
Wiestner A.,
Del Poeta G.,
Hartmann T.N.,
Gattei V.,
Zucchetto A.
Publication year - 2017
Publication title -
hematological oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 44
eISSN - 1099-1069
pISSN - 0278-0232
DOI - 10.1002/hon.2437_98
Subject(s) - chronic lymphocytic leukemia , breakpoint cluster region , ibrutinib , flow cytometry , medicine , immunology , context (archaeology) , in vivo , lymphocyte , leukemia , cancer research , chemistry , receptor , biology , paleontology , microbiology and biotechnology
zygosity in 60% of cases. The most frequent genetic losses involved CDKN2A/2B, TNFAIP3/A20, PRDM1, TCF3 and CIITA. The high recurrence of specific gene mutations such as MYD88 and the absence of mutations of KMT2D or FOXO1 are distinct features from nodal DLBCLs of either GC or ABC subtypes. Interestingly PCLBCL‐LT exhibits a mutational pattern that is closer to PCNSL than to ABC‐type nodal DLBCL but also has distinctive features, such as a very high mutational rate for PIM1, a higher rate of CD79B mutations and other original mutations such as CREBBP,MYC and IRF4 mutations (figure 1). Conclusion: This study describes for the first time the genomic landscape of a series of untreated PCLBCL‐LT. Our results obtained by WES and targeted sequencing underscore several similarities with ABC‐DBCL and more specifically with PCNSL subtypes. On the other hand, we pinpoint specificities that may sustain distinctive clinical features and guide therapeutic strategies according to an individual genetic analysis.