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Objective: This study aimed to summarize the clinical characteristics and prognosis of 108 patients with Waldenström macroglobulinemia (WM) in a single center and compare them with those of the Pivotal study with Bruton's tyrosine kinase inhibitor (BTKi) monotherapy. Methods: The clinical characteristics, international prognostic index score (IPSS) , first-line treatment, progression-free survival (PFS) , and overall survival (OS) of 108 patients with newly diagnosed WM from March 2008 to February 2021 were retrospectively evaluated. The MYD88 mutation was tested among 52 patients. Results: The median age of the 108 patients was 63 years (range, 38-78 years) with a male-to-female ratio of 3.5∶1. According to IPSS, we included 40% ( n =43) high-risk, 33% ( n =36) intermediate-risk, and 27% ( n =29) low-risk patients. In this study, no significant difference was observed in age, gender, IPSS risk, serum immunoglobulin M (IgM) , and platelet counts compared to the baseline characteristics of 63 patients in the pivotal study. However, hemoglobin (86 g/L vs 105 g/L) , serum β(2)-MG (3.1 mg/L vs 3.9 mg/L) , bone marrow involvement (13% vs 60%) , and the proportion of adenopathy (41% vs 59%) were significantly lower than those in the Pivotal group. The proportion of patients with splenomegaly (27% vs 11%) was significantly higher than that of the Pivotal group. All the differences were statistically different (all P values <0.05) . The overall positive rate of MYD88 mutation was 77%. With a median follow-up of 36 (1-121) months, the median OS was 95 months, and the median PFS was 35 months. The 2-year OS rate (83% vs 96%) and 5-year OS rate (67% vs 87%) of patients with WM in our center were lower than those in the Pivotal group. The proportion of novel treatments based on BTKi, CD20 monoclonal antibody, and proteasome inhibitors in our center from 2008 to 2021 has gradually increased from 50% to 93%. The long-term OS of patients diagnosed in 2015-2021 was improved compared with that in 2008-2014 ( P =0.048) . Conclusions: Novel drugs, including BTKi, continue to benefit patients with WM and improve their survival. It is worthwhile to further explore the positivity of MYD88 and CXCR4 mutations in the Chinese population and their sensitivity to BTKi.

Objective: The clinical characteristics of patients with primary central nervous system lymphoma-diffuse large B-cell lymphoma (PCNSL-DLBCL) and the effects of different treatment schemes on their survival and prognosis were analyzed retrospectively. Methods: A total of 49 patients with PCNSL-DLBCL who presented at the Tianjin Medical University General Hospital from July 2014 to December 2020 were included, and their clinical data were retrospectively analyzed. They were divided into four groups: the MTX group, the R-CDOP group, the BTKi-R-MTX group, and the RLZT group. The median overall survival (OS) and progression-free survival (PFS) were calculated, and the survival prognosis was compared by univariate and multivariate prognostic analysis. Results: The median OS time of the MTX group, the R-CDOP group, the BTKi-R-MTX group, and the RLZT group was 16.5 months, 4.5 months, 42 months, and not reached, respectively ( P <0.001) . The median PFS time of the MTX group, the R-CDOP group, the BTKi-R-MTX group, and the RLZT group was 7 months, 1.5 months, 20 months, and 5 months, respectively ( P =0.005) . Multivariate prognostic analysis showed that double expressor lymphoma, IESLG risk grade, and different treatment methods were the prognostic factors of PCNSL-DLBCL. Conclusion: The survival and prognosis of PCNSL-DLBCL are affected by different treatment schemes. The role of CD20 monoclonal antibody in the treatment of PCNSL-DLBCL is still controversial. The treatment scheme containing BTKi has great potential for PCNSL-DLBCL. RLZT scheme has a good prospect for elderly patients who cannot tolerate high-dose chemotherapy and radiotherapy.

Objective: To observe the effect of Bruton's tyrosine kinase (BTK) on the proliferation and differentiation of osteoclasts and to explore the mechanism of BTK on bone destruction in periapical periodontitis., Methods: After RAW264.7 cells induced with 100 ng·L⁻¹ receptor activator for nuclear factor-κB ligand (RANKL) for 5 days, osteoclast induction was confirmed by light microscopy, tartrate-resistant acid phosphatase (TRAP) staining, and quantitative real-time PCR (RT-qPCR). Then, BTK-small interfering RNA (BTK-siRNA) was transfected into cells induced for 5 days. After 24 h, the expression of TRAP mRNA was measured using RT-qPCR, and the proliferation and differentiation of osteoclasts were detected using CCK-8 and TRAP activity assay. Statistical analysis was performed., Results: After RAW264.7 was induced with RANKL for 5 days, a large number of round, ellipse, irregularly protuberant, and TRAP-positive macrophages were observed under light microscopy. The expression of TRAP mRNA significantly reduced after 24 h of BTK-siRNA transfection (P<0.05). The detection of CCK-8 and TRAP activities showed that the proliferation and differentiation of osteoclasts significantly decreased (P<0.05)., Conclusions: Silencing of BTK can inhibit the proliferation and differentiation of osteoclasts. BTK can be used as a new target for the inhibition of osteoclasts.