Department of Dermatology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
J Invest Dermatol. 2018 Nov;138(11):2365-2376. doi: 10.1016/j.jid.2018.04.038. Epub 2018 May 30.
Cutaneous diffuse large B-cell lymphomas (DLBCLs) are aggressive lymphomas with a poor prognosis. To elucidate their genetic bases, we analyzed exome sequencing of 37 cutaneous DLBCLs, including 31 DLBCLs, leg type (DLBCL-LT) and 6 cutaneous DLBCLs-not otherwise specified (DLBCL-NOS). As reported previously, 77% of DLBCL-LT harbor NF-κB-activating MYD88 mutations. In nearly all MYD88-wild-type DLBCL-LT, we found cancer-promoting mutations that either activate the NF-κB pathway through alternative genes (NFKBIE or REL) or activate other canonical cancer pathways (BRAF, MED12, PIK3R1, and STAT3). After NF-κB, the second most commonly mutated pathway putatively enables immune evasion via mutations predicted to downregulate antigen processing (B2M, CIITA, HLA) or T-cell co-stimulation (CD58). DLBCL-LT have little genetic overlap with the genetically heterogeneous DLBCL-NOS. Instead, they resemble primary central nervous system and testicular large B-cell lymphomas (primary central nervous system lymphomas and primary testicular lymphomas). Like primary central nervous system lymphomas/primary testicular lymphomas, 40% of DLBCL-LT (vs. 0% of DLBCLs-not otherwise specified) harbored PDL1/PDL2 translocations, which lead to overexpression of PD-L1 or PD-L2 in 50% of the cases. Collectively, these data broaden our understanding of cutaneous DLBCLs and suggest novel therapeutic approaches (e.g., BRAF or PI3K inhibitors). Additionally, they suggest novel treatment paradigms, wherein DLBCL-LT can be targeted with strategies (e.g., immune checkpoint blockers) currently being developed for genomically similar primary central nervous system lymphomas/primary testicular lymphomas.
皮肤弥漫性大 B 细胞淋巴瘤(DLBCL)是一种侵袭性强、预后差的淋巴瘤。为了阐明其遗传基础,我们对 37 例皮肤 DLBCL 进行了外显子组测序,包括 31 例 DLBCL-腿型(DLBCL-LT)和 6 例皮肤 DLBCL-非特指型(DLBCL-NOS)。如前所述,77%的 DLBCL-LT 存在 NF-κB 激活 MYD88 突变。在几乎所有 MYD88 野生型 DLBCL-LT 中,我们发现了促进癌症的突变,这些突变要么通过替代基因(NFKBIE 或 REL)激活 NF-κB 通路,要么激活其他经典的癌症通路(BRAF、MED12、PIK3R1 和 STAT3)。在 NF-κB 之后,第二个最常突变的途径可能通过预测下调抗原处理(B2M、CIITA、HLA)或 T 细胞共刺激(CD58)的突变来实现免疫逃逸。DLBCL-LT 与遗传异质性的 DLBCL-NOS 遗传重叠很少。相反,它们类似于原发性中枢神经系统和睾丸大 B 细胞淋巴瘤(原发性中枢神经系统淋巴瘤和原发性睾丸淋巴瘤)。与原发性中枢神经系统淋巴瘤/原发性睾丸淋巴瘤一样,40%的 DLBCL-LT(与 0%的 DLBCL-NOS 相比)存在 PDL1/PDL2 易位,导致 50%的病例中 PD-L1 或 PD-L2 过表达。总的来说,这些数据拓宽了我们对皮肤 DLBCL 的理解,并提出了新的治疗方法(例如,BRAF 或 PI3K 抑制剂)。此外,它们还提出了新的治疗方案,其中可以使用针对原发性中枢神经系统淋巴瘤/原发性睾丸淋巴瘤的类似基因的策略(例如免疫检查点抑制剂)来靶向治疗 DLBCL-LT。