Department of Veterinary Medicine and Surgery, University of Missouri, 900 E. Campus Drive, Columbia, MO, USA.
Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO, USA.
Epigenetics. 2022 Dec;17(13):2022-2038. doi: 10.1080/15592294.2022.2105033. Epub 2022 Jul 31.
Few recurrent DNA mutations are seen in aggressive canine B cell lymphomas (cBCL), suggesting other frequent drivers. The methylated island recovery assay (MIRA-seq) or methylated CpG-binding domain sequencing (MBD-seq) was used to define the genome-wide methylation profiles in aggressive cBCL in Golden Retrievers to determine if cBCL can be better defined by epigenetic changes than by DNA mutations. DNA hypermethylation patterns were relatively homogenous within cBCL samples in Golden Retrievers, in different breeds and in geographical regions. Aberrant hypermethylation is thus suspected to be a central and early event in cBCL lymphomagenesis. Distinct subgroups within cBCL in Golden Retrievers were not identified with DNA methylation profiles. In comparison, the methylome profile of human DLBCL (hDLBCL) is relatively heterogeneous. Only moderate similarity between hDLBCL and cBCL was seen and cBCL likely cannot be accurately classified into the subtypes seen in hDLBCL. Genes with hypermethylated regions in the promoter-TSS-first exon of cBCL compared to normal B cells often also had additional hyper- and hypomethylated regions distributed throughout the gene suggesting non-randomized repeat targeting of key genes by epigenetic mechanisms. The prevalence of hypermethylation in transcription factor families in aggressive cBCL may represent a fundamental step in lymphomagenesis.
在侵袭性犬 B 细胞淋巴瘤(cBCL)中很少观察到反复出现的 DNA 突变,这表明存在其他频繁的驱动因素。使用甲基化岛恢复分析(MIRA-seq)或甲基化 CpG 结合域测序(MBD-seq)来定义金毛猎犬中侵袭性 cBCL 的全基因组甲基化谱,以确定 cBCL 是否可以通过表观遗传变化而不是 DNA 突变得到更好的定义。在金毛猎犬、不同品种和不同地理区域的 cBCL 样本中,DNA 超甲基化模式相对同质。因此,异常超甲基化被怀疑是 cBCL 淋巴癌发生的核心和早期事件。在金毛猎犬的 cBCL 中没有发现具有 DNA 甲基化谱的不同亚组。相比之下,人类弥漫性大 B 细胞淋巴瘤(hDLBCL)的甲基组谱相对异质。仅在 hDLBCL 和 cBCL 之间观察到中度相似性,并且 cBCL 可能无法准确分类为 hDLBCL 中所见的亚型。与正常 B 细胞相比,cBCL 中在启动子-TSS-第一外显子中具有高甲基化区域的基因通常也具有分布在整个基因中的额外高甲基化和低甲基化区域,表明表观遗传机制对关键基因的非随机重复靶向。在侵袭性 cBCL 中转录因子家族中高甲基化的普遍性可能代表淋巴癌发生的一个基本步骤。