Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Department of Hematology, Tel-Aviv Sourasky (Ichilov) Medical Center, Tel Aviv, Israel.
Nat Med. 2021 Mar;27(3):491-503. doi: 10.1038/s41591-021-01232-w. Epub 2021 Feb 22.
Multiple myeloma (MM) is a neoplastic plasma-cell disorder characterized by clonal proliferation of malignant plasma cells. Despite extensive research, disease heterogeneity within and between treatment-resistant patients is poorly characterized. In the present study, we conduct a prospective, multicenter, single-arm clinical trial (NCT04065789), combined with longitudinal single-cell RNA-sequencing (scRNA-seq) to study the molecular dynamics of MM resistance mechanisms. Newly diagnosed MM patients (41), who either failed to respond or experienced early relapse after a bortezomib-containing induction regimen, were enrolled to evaluate the safety and efficacy of a daratumumab, carfilzomib, lenalidomide and dexamethasone combination. The primary clinical endpoint was safety and tolerability. Secondary endpoints included overall response rate, progression-free survival and overall survival. Treatment was safe and well tolerated; deep and durable responses were achieved. In prespecified exploratory analyses, comparison of 41 primary refractory and early relapsed patients, with 11 healthy subjects and 15 newly diagnosed MM patients, revealed new MM molecular pathways of resistance, including hypoxia tolerance, protein folding and mitochondria respiration, which generalized to larger clinical cohorts (CoMMpass). We found peptidylprolyl isomerase A (PPIA), a central enzyme in the protein-folding response pathway, as a potential new target for resistant MM. CRISPR-Cas9 deletion of PPIA or inhibition of PPIA with a small molecule inhibitor (ciclosporin) significantly sensitizes MM tumor cells to proteasome inhibitors. Together, our study defines a roadmap for integrating scRNA-seq in clinical trials, identifies a signature of highly resistant MM patients and discovers PPIA as a potent therapeutic target for these tumors.
多发性骨髓瘤(MM)是一种肿瘤性浆细胞疾病,其特征为恶性浆细胞的克隆性增殖。尽管进行了广泛的研究,但治疗抵抗患者的内在和外在疾病异质性仍描述不足。在本研究中,我们进行了一项前瞻性、多中心、单臂临床试验(NCT04065789),结合纵向单细胞 RNA 测序(scRNA-seq)研究 MM 耐药机制的分子动力学。新诊断的 MM 患者(41 例),在用硼替佐米为基础的诱导方案治疗后无反应或早期复发,入组评估达雷妥尤单抗、卡非佐米、来那度胺和地塞米松联合治疗的安全性和有效性。主要临床终点为安全性和耐受性。次要终点包括总缓解率、无进展生存期和总生存期。治疗安全且耐受良好;实现了深度和持久缓解。在预设的探索性分析中,将 41 例原发耐药和早期复发患者与 11 例健康受试者和 15 例新诊断的 MM 患者进行比较,发现了新的 MM 耐药分子途径,包括缺氧耐受、蛋白质折叠和线粒体呼吸,这些途径推广到更大的临床队列(CoMMpass)。我们发现肽基脯氨酰异构酶 A(PPIA),即蛋白质折叠反应途径的中心酶,是耐药 MM 的一个潜在新靶点。CRISPR-Cas9 敲除 PPIA 或用小分子抑制剂(环孢素)抑制 PPIA,可显著增加 MM 肿瘤细胞对蛋白酶体抑制剂的敏感性。综上所述,本研究为将 scRNA-seq 整合到临床试验中定义了路线图,确定了高度耐药 MM 患者的特征,并发现 PPIA 是这些肿瘤的有效治疗靶点。