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- Title
STAT3 Mutation Is Associated with STAT3 Activation in CD30+ ALK− ALCL.
- Authors
Andersson, Emma I.; Brück, Oscar; Braun, Till; Mannisto, Susanna; Saikko, Leena; Lagström, Sonja; Ellonen, Pekka; Leppä, Sirpa; Herling, Marco; Kovanen, Panu E.; Mustjoki, Satu
- Abstract
Peripheral T-cell lymphomas (PTCL) are a heterogeneous, and often aggressive group of non-Hodgkin lymphomas. Recent advances in the molecular and genetic characterization of PTCLs have helped to delineate differences and similarities between the various subtypes, and the JAK/STAT pathway has been found to play an important oncogenic role. Here, we aimed to characterize the JAK/STAT pathway in PTCL subtypes and investigate whether the activation of the pathway correlates with the frequency of STAT gene mutations. Patient samples from AITL (n = 30), ALCL (n = 21) and PTCL-NOS (n = 12) cases were sequenced for STAT3, STAT5B, JAK1, JAK3, and RHOA mutations using amplicon sequencing and stained immunohistochemically for pSTAT3, pMAPK, and pAKT. We discovered STAT3 mutations in 13% of AITL, 13% of ALK+ ALCL, 38% of ALK− ALCL and 17% of PTCL-NOS cases. However, no STAT5B mutations were found and JAK mutations were only present in ALK- ALCL (15%). Concurrent mutations were found in all subgroups except ALK+ ALCL where STAT3 mutations were always seen alone. High pY-STAT3 expression was observed especially in AITL and ALCL samples. When studying JAK-STAT pathway mutations, pY-STAT3 expression was highest in PTCLs harboring either JAK1 or STAT3 mutations and CD30+ phenotype representing primarily ALK− ALCLs. Further investigation is needed to elucidate the molecular mechanisms of JAK-STAT pathway activation in PTCL.
- Subjects
ANIMAL experimentation; CARRIER proteins; CELLULAR signal transduction; GENE expression; IMMUNOHISTOCHEMISTRY; IMMUNOPHENOTYPING; GENETIC mutation; ONCOGENES; STAT proteins; JANUS kinases
- Publication
Cancers, 2020, Vol 12, Issue 3, p702
- ISSN
2072-6694
- Publication type
Article
- DOI
10.3390/cancers12030702