Mulet-Lazaro Roger, Delwel Ruud
Department of Hematology, Erasmus MC Cancer Institute, University Medical Center Rotterdam, Rotterdam, the Netherlands.
Oncode Institute, Utrecht, the Netherlands.
Blood Cancer Discov. 2025 May 5;6(3):149-152. doi: 10.1158/2643-3230.BCD-25-0075.
The role of the proto-oncogene MYC as a driver of lymphoma has been known since the 1980s, but the mechanisms underlying its dysregulation are not completely understood. In this issue of Blood Cancer Discovery, Iyer and colleagues employ a CRISPR interference screen targeted at open chromatin regions to unveil enhancers critical for MYC overexpression in lymphoma, including a novel regulatory element in the MYC locus that controls germinal center reentry and is recurrently amplified in diffuse large B-cell lymphomas (germinal center B-cell diffuse large B-cell lymphoma). See related article by Iyer et al., p. 233.
自20世纪80年代以来，原癌基因MYC作为淋巴瘤驱动因子的作用就已为人所知，但其失调的潜在机制尚未完全明确。在本期《血癌发现》中，伊耶及其同事利用针对开放染色质区域的CRISPR干扰筛选，揭示了淋巴瘤中对MYC过表达至关重要的增强子，包括MYC基因座中的一个新型调控元件，该元件控制生发中心再进入，且在弥漫性大B细胞淋巴瘤（生发中心B细胞弥漫性大B细胞淋巴瘤）中反复扩增。见伊耶等人的相关文章，第233页。
