Department of Pathology, University of Cambridge, Cambridge, UK.
Haematological Malignancy Diagnostic Service, St James' University Hospital, Leeds, UK.
Leukemia. 2020 May;34(5):1329-1341. doi: 10.1038/s41375-019-0691-6. Epub 2019 Dec 16.
Using a Burkitt lymphoma-like gene expression signature, we recently defined a high-risk molecular high-grade (MHG) group mainly within germinal centre B-cell like diffuse large B-cell lymphomas (GCB-DLBCL), which was enriched for MYC/BCL2 double-hit (MYC/BCL2-DH). The genetic basis underlying MHG-DLBCL and their aggressive clinical behaviour remain unknown. We investigated 697 cases of DLBCL, particularly those with MYC/BCL2-DH (n = 62) by targeted sequencing and gene expression profiling. We showed that DLBCL with MYC/BCL2-DH, and those with BCL2 translocation, harbour the characteristic mutation signatures that are associated with follicular lymphoma and its high-grade transformation. We identified frequent MYC hotspot mutations that affect the phosphorylation site (T58) and its adjacent amino acids, which are important for MYC protein degradation. These MYC mutations were seen in a subset of cases with MYC translocation, but predominantly in those of MHG. The mutations were more frequent in double-hit lymphomas with IG as the MYC translocation partner, and were associated with higher MYC protein expression and poor patient survival. DLBCL with MYC/BCL2-DH and those with BCL2 translocation alone are most likely derived from follicular lymphoma or its precursor lesion, and acquisition of MYC pathogenic mutations may augment MYC function, resulting in aggressive clinical behaviour.
利用伯基特淋巴瘤样基因表达特征,我们最近定义了一个高风险分子高级(MHG)组,主要存在于生发中心 B 细胞样弥漫性大 B 细胞淋巴瘤(GCB-DLBCL)中,该组富含 MYC/BCL2 双重打击(MYC/BCL2-DH)。MHG-DLBCL 的遗传基础及其侵袭性临床行为尚不清楚。我们通过靶向测序和基因表达谱分析研究了 697 例 DLBCL,特别是那些具有 MYC/BCL2-DH(n=62)的病例。我们表明,具有 MYC/BCL2-DH 的 DLBCL 和具有 BCL2 易位的 DLBCL 具有与滤泡性淋巴瘤及其高级转化相关的特征性突变特征。我们发现了频繁的 MYC 热点突变,这些突变影响 MYC 蛋白降解的磷酸化位点(T58)及其相邻氨基酸。这些 MYC 突变可见于一部分具有 MYC 易位的病例中,但主要见于 MHG 病例中。这些突变在具有 IG 作为 MYC 易位伙伴的双重打击淋巴瘤中更为频繁,与更高的 MYC 蛋白表达和较差的患者生存相关。具有 MYC/BCL2-DH 和单独 BCL2 易位的 DLBCL 最有可能源自滤泡性淋巴瘤或其前体病变,并且获得 MYC 致病性突变可能增强 MYC 功能,导致侵袭性临床行为。