布鲁顿酪氨酸激酶抑制剂在B 细胞淋巴瘤中的研究进展*

Progression of Bruton tyrosine kinase (BTK) inhibitor in B-cell lymphoma

摘要: B 细胞受体（B -cell receptor，BCR ）信号通路在B 细胞肿瘤的发生、发展中起关键作用，其慢性持续的激活状态使正常细胞具备转化为恶性肿瘤细胞的能力。布鲁顿酪氨酸激酶（bruton tyrosine kinase ，BTK ）是非受体型酪氨酸激酶TEC 家族的一员，在BCR 信号通路的活化过程中起着关键的作用。通过BTK 小分子抑制剂调控BCR 信号转导，已经成为治疗某些B 细胞淋巴瘤的新靶点，并为B 细胞非霍奇金淋巴瘤（B-cell non-Hodgkin's lymphoma，B-NHL）的治疗带来新突破。本文将对现有BTK 小分子抑制剂在临床上的应用现状作一综述。

Abstract: Chronic activation of the B-cell antigen receptor (BCR) signaling pathway performs a critical function in the pathogenesis of numerous subtypes of B-cell malignancies and transforms normal cells into malignant cells. Bruton tyrosine kinase (BTK) is a member of the TEC family of tyrosine kinases and is a key regulator of the BCR signaling pathway. BTK inhibition has emerged as a new target for therapeutic intervention in B-cell malignancies. This review summarizes recent developments of BTK inhibitors in B-cell malignan -cies.