<p>T cell non-Hodgkin lymphomas (T-NHLs) represent a heterogeneous group of aggressive cancers of mature CD4+ T cells, for which therapeutic options are limited. Recent work uncovered that the <a href="https://www.ncbi.nlm.nih.gov/gene/5133">PDCD1</a> encoded immune checkpoint receptor PD-1 is a key tumor suppressor in T cells. PD-1 is recurrently inactivated in T-NHL and the highest frequencies of PDCD1 deletions are detected in advanced disease, predicting worse prognosis. The tumor-suppressive mechanisms of PD-1 signaling remain unknown. In the present study, we identify transcriptional and epigenetic mechanisms underlying PD-1 tumor suppression in T-NHL.</p><p>Some subjects included in this study overlap with the subjects from phs002456. To establish the link between the overlapping subjects, the Subject Consent datasets will be utilized.</p>

PD-1 Instructs a Tumor Suppressive Metabolic Program to Restrain AP-1    Activity in T Cell Lymphoma

Lymphoma, T-Cell, Cutaneous study with ATAC-seq, RNA-Seq + 1 more data on dbGaP (11 participants)

PD-1 Instructs a Tumor Suppressive Metabolic Program to Restrain AP-1 Activity in T Cell Lymphoma

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