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Alterations of negative regulators of cytokine signalling in immunodeficiency‐related non‐Hodgkin lymphoma
Author(s) -
Capello Daniela,
Gloghini Annunziata,
Baldanzi Gianluca,
Martini Maurizio,
Deambrogi Clara,
Lucioni Marco,
Piranda Daniela,
Famà Rosella,
Graziani Andrea,
Spina Michele,
Tirelli Umberto,
Paulli Marco,
Larocca Luigi Maria,
Gaidano Gianluca,
Carbone Antonino,
Sinigaglia Fabiola
Publication year - 2013
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.2010
Subject(s) - cancer research , socs3 , biology , suppressor of cytokine signaling 1 , jak stat signaling pathway , protein tyrosine phosphatase , janus kinase , stat protein , somatic hypermutation , suppressor of cytokine signalling , signal transduction , tyrosine kinase , genetics , stat3 , b cell , gene , suppressor , antibody
We investigated immunodeficiency‐related non‐Hodgkin lymphoma for the presence of molecular alterations affecting negative regulators of the Janus family protein tyrosine kinase/signal transducer and activator of transcription pathway. Protein tyrosine phosphatase, non‐receptor type 6/Src homology 2‐containing tyrosine phosphatase‐1 epigenetic silencing was recurrent in primary effusion lymphoma (100%), and diffuse large B‐cell lymphoma (63%), with a higher prevalence in the non‐germinal centre subtype, and was associated with the activation of the Janus family protein tyrosine kinase/signal transducer and activator of transcription 3 pathway. Suppressor of cytokine signalling ( SOCS )1 and SOCS3 epigenetic silencing were occasionally detected, whereas SOCS1 was frequently mutated in diffuse large B‐cell lymphoma and polymorphic post‐transplant lymphoproliferative disorders, possibly as a cause of aberrant somatic hypermutation. However, the mutation profile of the coding region of the gene was different from that expected from the aberrant somatic hypermutation process, suggesting that, at least in some cases, SOCS1 mutations may have been selected for their functional activity. Copyright © 2012 John Wiley & Sons, Ltd.