“…Moreover, inhibition of S100A8 could improve chemotherapy sensitivity by reducing autophagy in B-cell lymphoma cells with strong drug resistance (25). Simultaneously, S100A8/S100A9 activation facilitates leukocyte recruitment, angiogenesis, and tumor migration, along with the enhancement of some genes, including Cxcl1, Ccl5 and Ccl7, Slc39a10, Lcn2, Zc3h12a, Enpp2 and other genes (26,27). Generally, the role of S100A8 in multiple tumors is highlighted as a promotor of tumor invasion, TME formation, and drug resistance (14,16,28), however, there has been no direct report on relationship between S100A8 and DLBCL.…”