B cell receptor (BCR) signalling is crucial for normal B cell development and adaptive immunity. BCR signalling also supports the survival and growth of malignant B cells in patients with B cell leukaemias or lymphomas. The mechanism of BCR pathway activation in these diseases includes continuous BCR stimulation by microbial antigens or autoantigens present in the tissue microenvironment, activating mutations within the BCR complex or downstream signalling components and ligand-independent tonic BCR signalling. The most established agents targeting BCR signalling are Bruton tyrosine kinase (BTK) inhibitors and PI3K isoform-specific inhibitors, and their introduction into the clinic is rapidly changing how B cell malignancies are treated. B cells and BCR-related kinases, such as BTK, also play a role in the microenvironment of solid tumours, such as squamous cell carcinoma and pancreatic cancer, and therefore targeting B cells or BCR-related kinases may have anticancer activity beyond B cell malignancies.

B细胞受体（BCR）信号对于正常B细胞​​发育和适应性免疫至关重要。BCR信号传导还支持恶性B细胞在B细胞白血病或淋巴瘤患者中的存活和生长。在这些疾病中，BCR途径激活的机制包括组织微环境中存在的微生物抗原或自身抗原对BCR的持续刺激，激活BCR复合体或下游信号传导成分内的突变以及与配体无关的强直性BCR信号传导。靶向BCR信号的最成熟的药物是Bruton酪氨酸激酶（BTK）抑制剂和PI3K异构体特异性抑制剂，它们被引入临床正在迅速改变B细胞恶性肿瘤的治疗方式。B细胞和BCR相关激酶（例如BTK）也在实体瘤的微环境中发挥作用，