Lin Wuqiang, Chen Xiuli, Zheng Heyong, Cai Zhenjie
Department of Hematology, The First Hospital of Putian City, Putian, People's Republic of China.
Hematology. 2023 Dec;28(1):2231741. doi: 10.1080/16078454.2023.2231741.
Cell division cycle 37 (CDC37) modulates disease progression and bortezomib resistance in multiple myeloma by regulating X-box binding protein 1, nuclear factor-kappa-B, etc. This study aimed to explore the prognostic implication of CDC37 before and after bortezomib-based induction treatment in multiple myeloma patients.
CDC37 was detected from plasma cells of bone marrow by reverse transcription-quantitative polymerase chain reaction at baseline and after bortezomib-based induction treatment in 82 multiple myeloma patients, and in 20 disease controls and 20 healthy controls.
CDC37 was increased in multiple myeloma patients versus disease controls and healthy controls (both < 0.001). In multiple myeloma patients, CDC37 was related to increased serum creatinine (= 0.017) and beta-2-microglobulin (= 0.027), as well as unfavorable revised International Staging System stage (= 0.041). Notably, CDC37 was reduced after bortezomib-based induction treatment versus that at baseline (< 0.001). Furthermore, CDC37 at baseline was reduced in patients who achieved complete response versus those who did not achieve that (= 0.023). Additionally, CDC37 after bortezomib-based induction treatment was also decreased in patients who achieved complete response (< 0.001) and objective response (= 0.001) versus those who did not reach them. Meanwhile, CDC37 at baseline only predicted worse progression-free survival (= 0.033). Notably, CDC37 after bortezomib-based induction treatment estimated both shorter progression-free survival (= 0.006) and overall survival (= 0.005), which was confirmed by multivariate regression analysis.
CDC37 decreases after bortezomib-based induction treatment, while its higher expression reflects unsatisfactory induction treatment response and survival in multiple myeloma.
细胞分裂周期37（CDC37）通过调节X盒结合蛋白1、核因子-κB等，调控多发性骨髓瘤的疾病进展和硼替佐米耐药性。本研究旨在探讨基于硼替佐米的诱导治疗前后，CDC37在多发性骨髓瘤患者中的预后意义。
采用逆转录定量聚合酶链反应，在82例多发性骨髓瘤患者接受基于硼替佐米的诱导治疗前后，以及20例疾病对照者和20例健康对照者的骨髓浆细胞中检测CDC37。
与疾病对照者和健康对照者相比，多发性骨髓瘤患者的CDC37升高（均P<0.001）。在多发性骨髓瘤患者中，CDC37与血清肌酐升高（P=0.017）、β2微球蛋白升高（P=0.027）以及国际分期系统修订分期不佳（P=0.041）相关。值得注意的是，与基线时相比，基于硼替佐米的诱导治疗后CDC37降低（P<0.001）。此外，达到完全缓解的患者基线时的CDC37低于未达到完全缓解的患者（P=0.023）。此外，达到完全缓解（P<0.001）和客观缓解（P=0.001）的患者，基于硼替佐米的诱导治疗后的CDC37也低于未达到这些缓解的患者。同时，仅基线时的CDC37可预测无进展生存期较差（P=0.033）。值得注意的是，基于硼替佐米的诱导治疗后的CDC37可预测较短的无进展生存期（P=0.006）和总生存期（P=0.005），多因素回归分析证实了这一点。
基于硼替佐米的诱导治疗后CDC37降低，而其较高表达反映了多发性骨髓瘤诱导治疗反应和生存情况不佳。
