决定异体 CAR T 细胞排斥与扩增的细胞和分子机制
Cellular and molecular mechanisms determining allogeneic CAR T cell rejection and expansion.
我们评估了11例接受单一批次cemacabtagene ansegedleucel(cema-cel)治疗的大B细胞淋巴瘤患者,cemacabtagene ansegedleucel是一种异体抗CD19 CAR T产品。
英文原题:SOHO State of the Art Updates and Next Questions | Peripheral T-Cell Lymphoma: Current Landscape and Emerging Questions.
外周T细胞淋巴瘤(PTCLs)是一组罕见的、异质性的成熟T细胞和NK细胞肿瘤,约占所有非霍奇金淋巴瘤的10%至15%。
外周T细胞淋巴瘤(PTCLs)是一组罕见的、异质性的成熟T细胞和NK细胞肿瘤,约占所有非霍奇金淋巴瘤的10%至15%。尽管在疾病分类和生物学方面取得了进展,但除间变性淋巴瘤激酶(ALK)阳性的间变性大细胞淋巴瘤(ALCL)外,大多数亚型的临床结局仍然不佳。本综述综合了目前对结内PTCL生物学的认识——包括T细胞滤泡辅助(TFH)来源的淋巴瘤、PTCL-NOS和系统性ALCL。分子谱分析的整合加深了我们对疾病异质性的理解,识别出反复出现的表观遗传和信号通路改变,这些改变如今为合理的靶向策略提供了依据。以维布妥昔单抗为基础的方案重塑了CD30阳性疾病的一线治疗,而正在进行的研究正在探索新型疗法在PTCL谱系中的作用,包括表观遗传调节剂、磷脂酰肌醇3-激酶(PI3K)和JAK抑制剂以及免疫基础疗法。未来的进展将取决于生物标志物驱动的临床试验、精细化的患者选择,以及整合基因组和免疫特征以实现个体化治疗。
Peripheral T-cell lymphomas (PTCLs) comprise a rare, heterogeneous group of mature T-cell and NK-cell neoplasms, representing approximately 10% to 15% of all non-Hodgkin lymphomas. Despite advances in disease classification and biology, clinical outcomes remain poor for most subtypes other than anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL). This review synthesizes current understanding of nodal PTCL biology-including T-cell follicular helper (TFH)-derived lymphomas, PTCL-NOS, and systemic ALCL. The integration of molecular profiling has deepened our understanding of disease heterogeneity, identifying recurrent epigenetic and signaling pathway alterations that now inform rational, targeted strategies. Brentuximab vedotin-based regimens have reshaped frontline therapy for CD30-positive disease, while ongoing studies are exploring the role of novel therapies including epigenetic modulators, phosphatidylinositol 3-kinase (PI3K) and JAK inhibitors, and immune-based therapies across the PTCL spectrum. Future progress will depend on biomarker-driven clinical trials, refined patient selection, and the incorporation of genomic and immune signatures to personalize therapy.
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