Takahashi Kazuya, Inukai Takeshi, Imamura Toshihiko, Yano Mio, Tomoyasu Chihiro, Lucas David M, Nemoto Atsushi, Sato Hiroki, Huang Meixian, Abe Masako, Kagami Keiko, Shinohara Tamao, Watanabe Atsushi, Somazu Shinpei, Oshiro Hiroko, Akahane Koshi, Goi Kumiko, Kikuchi Jiro, Furukawa Yusuke, Goto Hiroaki, Minegishi Masayoshi, Iwamoto Shotaro, Sugita Kanji
Department of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
PLoS One. 2017 Dec 13;12(12):e0188680. doi: 10.1371/journal.pone.0188680. eCollection 2017.
Prognosis of childhood acute lymphoblastic leukemia (ALL) has been dramatically improved. However, prognosis of the cases refractory to primary therapy is still poor. Recent phase 2 study on the efficacy of combination chemotherapy with bortezomib (BTZ), a proteasome inhibitor, for refractory childhood ALL demonstrated favorable clinical outcomes. However, septic death was observed in over 10% of patients, indicating the necessity of biomarkers that could predict BTZ sensitivity. We investigated in vitro BTZ sensitivity in a large panel of ALL cell lines that acted as a model system for refractory ALL, and found that Philadelphia chromosome-positive (Ph+) ALL, IKZF1 deletion, and biallelic loss of CDKN2A were associated with favorable response. Even in Ph-negative ALL cell lines, IKZF1 deletion and bilallelic loss of CDKN2A were independently associated with higher BTZ sensitivity. BTZ showed only marginal cross-resistance to four representative chemotherapeutic agents (vincristine, dexamethasone, l-asparaginase, and daunorubicin) in B-cell precursor-ALL cell lines. To improve the efficacy and safety of proteasome inhibitor combination chemotherapy, we also analyzed the anti-leukemic activity of carfilzomib (CFZ), a second-generation proteasome inhibitor, as a substitute for BTZ. CFZ showed significantly higher activity than BTZ in the majority of ALL cell lines except for the P-glycoprotein-positive t(17;19) ALL cell lines, and IKZF1 deletion was also associated with a favorable response to CFZ treatment. P-glycoprotein inhibitors effectively restored the sensitivity to CFZ, but not BTZ, in P-glycoprotein-positive t(17;19) ALL cell lines. P-glycoprotein overexpressing ALL cell line showed a CFZ-specific resistance, while knockout of P-glycoprotein by genome editing with a CRISPR/Cas9 system sensitized P-glycoprotein-positive t(17;19) ALL cell line to CFZ. These observations suggested that IKZF1 deletion could be a useful biomarker to predict good sensitivity to CFZ and BTZ, and that CFZ combination chemotherapy may be a new therapeutic option with higher anti-leukemic activity for refractory ALL that contain P-glycoprotein-negative leukemia cells.
儿童急性淋巴细胞白血病(ALL)的预后已得到显著改善。然而,对初始治疗耐药的病例预后仍然很差。最近一项关于蛋白酶体抑制剂硼替佐米(BTZ)联合化疗对难治性儿童ALL疗效的2期研究显示出良好的临床结果。然而,超过10%的患者出现败血症死亡,这表明需要能够预测BTZ敏感性的生物标志物。我们在一大组ALL细胞系中研究了体外BTZ敏感性,这些细胞系作为难治性ALL的模型系统,发现费城染色体阳性(Ph+)ALL、IKZF1缺失和CDKN2A双等位基因缺失与良好反应相关。即使在Ph阴性ALL细胞系中,IKZF1缺失和CDKN2A双等位基因缺失也与较高的BTZ敏感性独立相关。在B细胞前体ALL细胞系中,BTZ对四种代表性化疗药物(长春新碱、地塞米松、L-天冬酰胺酶和柔红霉素)仅表现出轻微的交叉耐药性。为了提高蛋白酶体抑制剂联合化疗的疗效和安全性,我们还分析了第二代蛋白酶体抑制剂卡非佐米(CFZ)作为BTZ替代品的抗白血病活性。除P-糖蛋白阳性的t(17;19) ALL细胞系外,CFZ在大多数ALL细胞系中显示出比BTZ显著更高的活性,并且IKZF1缺失也与CFZ治疗的良好反应相关。P-糖蛋白抑制剂有效地恢复了P-糖蛋白阳性的t(17;l9) ALL细胞系对CFZ的敏感性,但未恢复对BTZ的敏感性。P-糖蛋白过表达的ALL细胞系表现出对CFZ的特异性耐药,而通过CRISPR/Cas9系统进行基因组编辑敲除P-糖蛋白可使P-糖蛋白阳性的t(17;19) ALL细胞系对CFZ敏感。这些观察结果表明,IKZF1缺失可能是预测对CFZ和BTZ敏感性良好的有用生物标志物,并且CFZ联合化疗可能是一种对含有P-糖蛋白阴性白血病细胞的难治性ALL具有更高抗白血病活性的新治疗选择。