“…In addition, cytolytic activity, DCs, the inflammation-promoting process, neutrophils, and pDCs were clustered into the high-risk group which may provide novel immunotherapy targets which means the hypoxic TME may play a crucial role in pathogeneses and progression in DLBCL. Consistent with previous results, ECM-related features such as basement membrane, integrin binding, and focal adhesion were significantly enriched in the low-risk group based on GO and KEGG pathway analyses, indicating that these factors may be associated with better prognosis (Hou et al, 2022). We further speculated the possible therapeutic targets using the pRRophetic package and found that higher IC50 values of afatinib, bosutinib, ATRA, methotrexate, gemcitabine, veliparib, lenalidomide, GW843682X, etoposide, BI-D1870, and rucaparib, as well as reduced IC50 values of LFM-A13, A-770041, axitinib, lapitinib, imatinib, bryostatin.1, and doramapimod, were observed in the low immune score group which indicated that patients with a higher immune score presented higher sensitivity to afatinib, bosutinib, ATRA, methotrexate, gemcitabine, veliparib, lenalidomide, GW843682X, etoposide, BI-D1870, and rucaparib, as well as lower sensitivity to LFM-A13, A-770041, axitinib, lapitinib, imatinib, bryostatin.1, and doramapimod, and thus show better therapy sensitivity.…”