2021美国癌症研究学会年会速递:改善实体瘤过继性细胞疗法的新策略

2021-04-14 Oranhgy MedSci原创

美国癌症研究协会(AACR)成立于1907年,是世界上历史最久、规模最大的科学组织,是有关癌症的病因、诊断、治疗和预防进展的权威信息来源,专注于高质量,创新性癌症研究的各个方面。

美国癌症研究协会(AACR)成立于1907年,是世界上历史最久、规模最大的科学组织,是有关癌症的病因、诊断、治疗和预防进展的权威信息来源,专注于高质量,创新性癌症研究的各个方面。目前在127个国家拥有超过46000名会员,成员包括AACR学院的178名研究员、48位诺贝尔奖获得者。

2021年112届AACR年会于2021年4月10-15日在线举行。此次会议上提出了改善实体瘤过继细胞疗法新策略。

21世纪是细胞治疗的时代,肿瘤免疫疗法被称为继手术、放疗、化疗后的第四种肿瘤疗法。肿瘤免疫治疗策略主要包括四大类:过继性免疫细胞治疗、免疫检验点单克隆抗体治疗、肿瘤疫苗治疗、非特异性免疫刺激治疗(细胞因子治疗)。因此过继性细胞疗法(adoptive cell therapy,ACT)属于肿瘤免疫疗法的一个分支,是未来医学发展的重要方向之一。

过继性免疫细胞治疗是指从肿瘤患者体内分离免疫活性细胞,在体外进行扩增和功能鉴定,然后向患者回输,从而达到直接杀伤肿瘤或激发机体的免疫应答杀伤肿瘤细胞的目的。过继性免疫细胞治疗主要包括NK 、LAK、DC、CIK、CTL、TIL、、TCR-T、CAR-T等几大类。

从技术的角度看,随着更多肿瘤抗原靶点的开发以及细胞疗法的技术改进,CAR-T和TCR-T细胞治疗将成为主流的肿瘤治疗手段。

尽管CAR-T疗法在治疗血液学恶性肿瘤方面取得了显著的成功。然而,在治疗实体瘤方面仍然存在挑战,存在治疗分子无效地贩运到肿瘤,低效的激活、增殖以及治疗的耗尽等一系列。AACR会上,科学家们提出了不同的策略,帮助疗法解决该系列问题。

针对乳腺癌的MUC1*靶向CAR-T治疗

来自Minerva科技公司的Cynthia Bamdad博士讲述了针对转移性乳腺癌的CAR-T疗法,该疗法以MUC1*蛋白为靶点,是MUC1生长因子受体的裂解产物。MUC1在75%的实体瘤上都有异常表达,因此被认为是抗癌治疗的绝佳靶点。然而,之前开发任何疗法的尝试都失败了,主要原因是该蛋白的作用机制被误解。

Cynthia博士认为MUC1*靶向huMNC2-CAR44是单克隆抗体,能特异性地与癌细胞结合,不伤害正常细胞。将该疗法一次性注射到植入人类乳腺癌组织的小鼠体内,成功阻止癌症生长长达100天。

目前,该疗法正在弗雷德-哈奇癌症中心的乳腺癌首例人体1/2期试验中进行测试。到目前为止,已有3名患者接受评估,其中2名患者病情稳定,1名患者有部分反应。其中一名患者还表现出强大的CAR T扩张,在第155天的时候,CAR T细胞/ml血量达到8000个。

虽然CAR-T疗法已经取得了很高的疗效,但它们未能保持长期效果导致癌症缓解。部分原因是由于它们在体内的持久性差。

Cynthia博士还介绍了一种改良的CAR-T疗法--huMNC2-CAR-1XX的数据,这种疗法可以持续更长时间,并且对肿瘤生长有长期的负面影响。 在一项小鼠研究中,1XX CAR能够将表达MUC1*的肿瘤控制在83天之久。在这个时间点上,标准CAR已经开始分化和耗尽。此外,在组织切片中,1XX CAR清楚地显示出没有表达MUC1*的肿瘤细胞,而标准CAR则有大量的MUC1抗原代表。

异体、现成的NK细胞产品改善抗HER2胃癌治疗的疗效

免疫检查点和采用细胞疗法对治疗一些癌症非常有效,但对胃癌的治疗却不太成功。然而,一种新的重编程NK细胞方法非常有前途。NK细胞在癌症免疫监视中发挥着重要作用,并介导抗肿瘤和抗病毒反应。除了对转化细胞具有天然的细胞毒性外,NK细胞还可以分泌多种细胞因子和趋化因子,调节免疫微环境。因此,NK细胞在癌症治疗中具有巨大的潜力。

来自Celularity的Lin Kang博士介绍了一种基于NK细胞的产品CYNK-101,旨在增强和维持抗体依赖性细胞毒性反应(ADCC)。NK细胞上的CD16受体对ADCC很重要,然而,ADCC反应的亲和力和持久性取决于CD16的稳定性。CYNK-101是经过基因改造的NK细胞,其表达的CD16变体具有高亲和力和高稳定性,能促进NK细胞持续反应。

在该研究中,特别研究了CYNK-101与抗体治疗HER-2阳性胃癌的Trastuzumab联合治疗的疗效。该组合治疗具有高度的细胞毒性,这与IFN-gamma、TNF-a和GM-CSF等细胞毒性因子的释放增加是一致的,并且对胃癌细胞系具有很强的特异性。两种治疗方法在体外、体外和体内模型中均表现出协同作用。Celularity计划很快提交IND,进行1期试验,在HER2阳性胃癌中测试这一组合。

CAR-T与宿主免疫细胞之间的相互作用促进了强大的抗肿瘤反应

CAR-T细胞能有效杀死肿瘤,但并不是仅依靠自己来完成的。Mustang Bio的Christine Brown博士及其同事的一项研究阐明了CAR-T治疗刺激的宿主免疫对全面抗肿瘤反应的作用。

他们的研究表明,CAR-T治疗后胶质母细胞瘤患者提取的T细胞对肿瘤的反应性更强,产生更多的干扰素-gamma,杀伤肿瘤细胞的能力增强。此外,CAR-T治疗在小鼠中的抗肿瘤反应更优,小鼠具有功能性的、有能力的免疫系统,而不是免疫功能低下的小鼠。这说明CAR-T细胞可能刺激了内源性免疫反应。

此外,CAR-T还能产生针对肿瘤的记忆反应。当给CAR-T治疗后治愈癌症的小鼠注射缺乏CAR-T所针对的抗原的肿瘤细胞时,它们可以对抗肿瘤细胞。这说明CAR-T治疗能够产生新的T细胞反应,杀死之前免疫细胞未知的肿瘤。

CAR-T细胞能够激活肿瘤微环境中的内源性T细胞以及胶质母细胞瘤肿瘤中的常驻髓细胞群。此外,它们还诱导了与干扰素-gamma刺激相关基因的表达。发现干扰素-gamma的作用对CAR-T细胞的反应极为关键,因为干扰素-gamma缺乏的小鼠不能通过CAR-T疗法杀死肿瘤细胞。IFN阴性小鼠CAR-T反应的降低伴随着髓细胞活化和宿主T细胞活化的降低。

该研究表明,CAR-T治疗后出现的抗肿瘤反应不能仅仅归因于治疗。还受到其他因素的驱动,如内源性T细胞和肿瘤常驻巨噬细胞的激活,以及肿瘤附近IFN-gamma的产生。Brown博士认为:"生产性CAR-T细胞介导的内源性抗肿瘤免疫的诱导,可以产生多克隆免疫反应来解决肿瘤异质性和免疫学记忆,以减少潜在的肿瘤复发。"

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    2021-05-23 qjddjq
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    2021-04-22 科研科研科研

    改善实体瘤

    0

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    2021-04-15 科研科研科研

    实体瘤的治疗心策略

    0

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    2021-04-14 yangchou

    好文章,谢谢分享。

    0

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