Weiwei Zhang

TL;DR: The findings suggest that JAK-STAT pathway inhibition may represent a therapeutic strategy in NK/T-cell lymphomas and their cell lines through next generation and/or Sanger sequencing.

TL;DR: Target resequencing on 92 cases of PTCL and frequent mutations affecting RHOA, TET2, DNMT3A, and isocitrate dehydrogenase 2 (IDH2) revealed recurrently hypermethylated genes involved in T-cell receptor signaling and T- cell differentiation that likely contribute to lymphomagenesis in AITL.

TL;DR: It is demonstrated that novel GEP-defined PTCL subgroups likely evolve by distinct genetic pathways and provided biological rationale for therapies that may be investigated in future clinical trials.

TL;DR: Abnormalities associated with transformation of the disease likely impair immune surveillance, activate the nuclear factor-κB pathway, and deregulate p53 and B-cell transcription factors.

TL;DR: Recurrent mutations in CD28 are identified in peripheral T-cell lymphomas and found increased transcription of the CD28-responsive genes CD226 and TNFA in cells expressing the T195P mutant in response to CD3 and CD86 co-stimulation and increased downstream activation of NF-κB by both D124V and T 195P mutants, suggesting a potential therapeutic target inCD28-mutated PTCLs.