ATAC-seq data from murine peripheral T-cell lymphoma and control normal T cells, NKT cells and NK cells

Peripheral T-cell lymphomas (PTCLs) represent a significant unmet medical need with dismal clinical outcome.T-cell receptor (TCR) is emerging as a key driver of T lymphocytes transformation. However, the role of chronic TCR activation in lymphomagenesis and in survival of lymphoma cells is still poorly understood. Using an original mouse model, we report here that chronic TCR stimulation drives T-cell lymphomagenesis whereas TCR signaling does not contribute to PTCL survival. Epigenetic analyses of mouse PTCLs using ATAC-seq revealed a NK-like reprogramming of PTCL cells with increase accessibility to OCR associated with NK cells. Overall design: 18 samples. 9 mPTCLs generated after transfer of p53KO T cells into syngeneic recipient C57BL/6 CD3KO mice, 3 normal T cells, 3 normal NKT cells and 3 normal NK cells