染色体易位
生物
滤泡性淋巴瘤
BCL6公司
免疫球蛋白重链
癌症研究
淋巴瘤
造血
祖细胞
免疫球蛋白基因
基因重排
突变
基因
分子生物学
遗传学
B细胞
抗体
干细胞
免疫学
生发中心
作者
Sarah Haebe,William David Keay,Stefan Alig,Anne‐Wiebe Mohr,Larissa K. Martin,Michael Heide,Ramona Secci,Stefan Krebs,Helmut Blum,Andreas Moosmann,Abner Louissaint,David M. Weinstock,Silvia Thoene,Michael Bergwelt‐Baildon,Jürgen Ruland,Deepak Bararia,Oliver Weigert
摘要
Relapsed follicular lymphoma (FL) can arise from common progenitor cells (CPCs). Conceptually, CPC-defining mutations are somatic alterations shared by the initial and relapsed tumours, mostly B-cell leukaemia/lymphoma 2 (BCL2)/immunoglobulin heavy locus (IGH) translocations and other recurrent gene mutations. Through complementary approaches for highly sensitive mutation detection, we do not find CPC-defining mutations in highly purified BCL2/IGH-negative haematopoietic progenitor cells in clinical remission samples from three patients with relapsed FL. Instead, we find cells harbouring the same BCL2/IGH translocation but lacking CREB binding protein (CREBBP), lysine methyltransferase 2D (KMT2D) and other recurrent gene mutations. Thus, (i) the BCL2/IGH translocation can precede CPC-defining mutations in human FL, and (ii) BCL2/IGH-translocated cells can persist in clinical remission.
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