International Center for Cell Therapy and Cancer Immunotherapy (CTCI), Weizman Center, 14 Weizman Street, Tel Aviv, 64239, Israel.
Cancer Immunol Immunother. 2010 Oct;59(10):1511-9. doi: 10.1007/s00262-010-0878-1. Epub 2010 Jun 20.
The feasibility and safety of immunotherapy mediated by intentionally mismatched rIL-2 activated killer lymphocytes (IMAK) with no prior stem cell engraftment was investigated in patients with advanced chemotherapy-resistant hematological malignancies and metastatic solid tumors. Our goals were to maximize anti-cancer activity by using intentionally mismatched donor lymphocytes; amplify killing of target cancer cells by rIL-2 activation of killer cells in vitro and in vivo, and avoid the risk of graft-versus-host disease (GVHD) by anticipated rejection of alloreactive donor lymphocytes. Conditioning consisted of 5 days of fludarabine 25 mg/m(2) or a single dose of cyclophosphamide 1,000 mg/m(2), 2 subcutaneous injections of alpha interferon (IFN) 3 x 10(6) and COX2 inhibitors, followed by administration of IMAK (65 +/- 5 CD3(+)CD56(-); 17 +/- 5 CD3(-)CD56(+)) in conjunction with low dose subcutaneous rIL-2 (6 x 10(6) IU/m(2)/day) for 5 days for continuous activation of alloreactive donor lymphocytes prior to their anticipated rejection. Here, we present our phase 1 clinical study data in a cohort of 40 high-risk patients with metastatic solid tumors and hematological malignancies. Treatment was accompanied by some malaise and occasional self-limited fever but otherwise well tolerated on an outpatient basis. Transient engraftment of donor cells was documented in two patients and only one developed self-limited grade 1 GVHD. Among patients with chemotherapy-resistant disease, long-term progression-free survival was recorded in 5 of 21 evaluable patients with metastatic solid tumors and in four of five patients with hematological malignancies. We conclude that the proposed procedure is feasible, safe, and potentially effective, with some otherwise resistant cancer patients long-term disease-free, thus justifying larger Phase II studies in patients with hematological malignancies and metastatic solid tumors, preferably at a stage of minimal residual disease with the goal in mind to eradicate all malignant cells at an early stage of the disease.
本研究旨在探讨未经干细胞移植预先致敏的、与供者间存在遗传不匹配的重组白细胞介素 2 激活杀伤细胞(IMAK)介导的免疫治疗在晚期、对化疗耐药的血液恶性肿瘤和转移性实体瘤患者中的可行性和安全性。我们的目标是通过使用遗传不匹配的供者淋巴细胞来最大化抗肿瘤活性;通过体外和体内重组白细胞介素 2 激活杀伤细胞来扩增对靶癌细胞的杀伤;并通过预期排斥同种异体反应性供者淋巴细胞来避免移植物抗宿主病(GVHD)的风险。预处理方案包括:5 天氟达拉滨 25mg/m2 或单剂量环磷酰胺 1000mg/m2,2 次皮下注射α干扰素(IFN)3x106 和 COX2 抑制剂,随后给予 IMAK(65+/-5 CD3+CD56-;17+/-5 CD3-CD56+),并联合低剂量皮下重组白细胞介素 2(6x106IU/m2/天)连续激活同种异体反应性供者淋巴细胞,直至预期排斥。在此,我们报告了在 40 例具有转移性实体瘤和血液恶性肿瘤的高危患者中进行的 1 期临床研究数据。该治疗方案伴有一些不适和偶尔的自限性发热,但在门诊基础上可良好耐受。在两名患者中记录到供者细胞的短暂植入,仅 1 名患者发生自限性 1 级 GVHD。在对化疗耐药的患者中,21 例可评估的转移性实体瘤患者中有 5 例和 5 例血液恶性肿瘤患者中有 4 例记录到长期无进展生存。我们得出结论,该方案是可行的、安全的、有潜在疗效的,一些原本耐药的癌症患者长期无病生存,因此,在血液恶性肿瘤和转移性实体瘤患者中开展更大规模的 2 期研究是合理的,最好在疾病早期处于最小残留疾病阶段,目的是尽早消除所有恶性细胞。