肿瘤细胞治疗研究
英文原题：Resistance to Bruton tyrosine kinase inhibitors: the Achilles heel of their success story in lymphoid malignancies.
Bruton酪氨酸激酶抑制剂（BTKi）显著改变了B细胞恶性肿瘤患者的治疗格局，包括慢性淋巴细胞白血病、华氏巨球蛋白血症、套细胞淋巴瘤和边缘区淋巴瘤。
Bruton酪氨酸激酶抑制剂（BTKi）显著改变了B细胞恶性肿瘤患者的治疗格局，包括慢性淋巴细胞白血病、华氏巨球蛋白血症、套细胞淋巴瘤和边缘区淋巴瘤。遗憾的是，BTKi耐药患者的生存期缩短。临床和分子风险因素，如既往治疗次数和TP53突变的存在，可用于预测发生BTKi耐药风险最高的患者。已报道多种BTKi耐药机制，其中BTK和磷脂酶Cγ2突变拥有最多的数据支持。venetoclax的引入延长了BTKi耐药患者的生存期。正在进行的临床试验中，有前景的治疗方式，如新一代BTKi和CAR-T 细胞疗法，已在BTKi耐药患者中报告了令人鼓舞的疗效。需要继续开展聚焦于耐药机制及如何规避耐药的研究，以进一步延长BTKi耐药B细胞恶性肿瘤患者的生存期。
Bruton tyrosine kinase inhibitors (BTKi) have significantly changed the treatment landscape for patients with B-cell malignancies, including chronic lymphocytic leukemia, Waldenstrom macroglobulinemia, mantle cell lymphoma, and marginal zone lymphoma. Unfortunately, patients with BTKi-resistant disease have shortened survival. Clinical and molecular risk factors, such as number of prior therapies and presence of TP53 mutations, can be used to predict patients at the highest risk of developing BTKi resistance. Many mechanisms of BTKi resistance have been reported with mutations in BTK and phospholipase C γ2 supported with the most data. The introduction of venetoclax has lengthened the survival of patients with BTKi-resistant disease. Ongoing clinical trials with promising treatment modalities, such as next-generation BTKi and chimeric antigen receptor T-cell therapy, have reported promising efficacy in patients with BTKi-resistant disease. Continued research focusing on resistance mechanisms and methods of how to circumvent resistance is needed to further prolong the survival of patients with BTKi-resistant B-cell malignancies.
MEMBER ACCOUNT
登录成功会直接打开下一页。
