Myeloma Drug Resistance Induced by Binding of Myeloma B7-H1 (PD-L1) to PD-1.

B7 homolog 1 (B7-H1)-expressing myeloma cells not only inhibit myeloma-specific cytotoxic T lymphocytes (CTL), but also confer a proliferative advantage: resistance to antimyeloma chemotherapy. However, it remains unknown whether B7-H1 expressed on myeloma cells induces cellular responses associated with aggressive myeloma behaviors. To address this question, we analyzed the proliferation and drug sensitivity of B7-H1-expressing myeloma cells transfected with B7-H1-specific short-hairpin RNA or treated with programmed cell death (PD)-1-Fc-coupled beads.

[Evaluation of the enhanced International Prognostic Index (NCCN-IPI) for cases with diffuse large B-cell lymphoma].

The NCCN-International Prognostic Index (IPI) is reported to be more powerful than the former IPI for predicting survival in the rituximab era. To evaluate the NCCN-IPI in our institutions, we analyzed 188 patients with diffuse large B-cell lymphoma treated with rituximab plus CHOP or THP-COP chemotherapy. The 5-year overall survival rates of patients with low, low-intermediate, high-intermediate, and high risk were 90%, 76%, 64%, and 34%, respectively.