Pathogenic B-cell receptor signaling in lymphoid malignancies: New insights to improve treatment

被引：101

作者：

Young, Ryan M. ^{[1
]}

Phelan, Mes D. ^{[1
]}

Wilson, Wyndham H. ^{[1
]}

Staudt, Louis M. ^{[1
]}

机构：

[1] NCI, Lymphoid Malignancies Branch, Ctr Canc Res, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA

来源：

IMMUNOLOGICAL REVIEWS | 2019年 / 291卷 / 01期

关键词：

B-cell receptor; cancer; lymphoma; signal transduction; CHRONIC LYMPHOCYTIC-LEUKEMIA; NF-KAPPA-B; BRUTON TYROSINE KINASE; NON-HODGKIN-LYMPHOMA; HUMAN FOLLICULAR LYMPHOMA; L265P SOMATIC MUTATION; LYN-DEFICIENT MICE; GERMINAL CENTER; GENE-EXPRESSION; ACALABRUTINIB ACP-196;

D O I：

10.1111/imr.12792

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Signals emanating from the B-cell receptor (BCR) promote proliferation and survival in diverse forms of B-cell lymphoma. Precision medicine strategies targeting the BCR pathway have been generally effective in treating lymphoma, but often fail to produce durable responses in diffuse large B-cell lymphoma (DLBCL), a common and aggressive cancer. New insights into DLBCL biology garnered from genomic analyses and functional proteogenomic studies have identified novel modes of BCR signaling in this disease. Herein, we describe the distinct roles of antigen-dependent and antigen-independent BCR signaling in different subtypes of DLBCL. We highlight mechanisms by which the BCR cooperates with TLR9 and mutant isoforms of MYD88 to drive sustained NF-kappa B activity in the activated B-cell-like (ABC) subtype of DLBCL. Finally, we discuss progress in detecting and targeting oncogenic BCR signaling to improve the survival of patients with lymphoma.

引用

页码：190 / 213

页数：24

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