Kawai Hidetsugu, Iwata Shino, Shiraiwa Sawako, Miyaoka Masashi, Ogiya Daisuke, Toyosaki Masako, Machida Shinichiro, Suzuki Rikio, Onizuka Makoto, Ogawa Yoshiaki, Nakamura Naoya, Kawada Hiroshi
Department of Hematology / Oncology, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Department of Pathology, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
J Clin Exp Hematop. 2025;65(1):55-61. doi: 10.3960/jslrt.24048.
Severe atopic dermatitis (AD) is known to be associated with a risk of lymphoma. We herein report a case of ALK-negative anaplastic large cell lymphoma (ALK-ALCL) complicated by severe AD during treatment with baricitinib, which is an oral, selective, and reversible Janus Kinase (JAK) 1 and 2 inhibitor used in the treatment of AD. Next-generation sequencing (NGS) demonstrated the TP53 p.G266E mutation, suggesting that this was the trigger of the disease and the cause of its refractory course. The JAK/signal transducer and activator of transcription (STAT) pathway is often activated in tumor cells of ALCLs, suggesting that it is a therapeutic target. The causal connection between baricitinib and lymphomagenesis remains unknown; however, this patient developed ALK-ALCL with TP53 mutations during baricitinib treatment.
已知重度特应性皮炎(AD)与淋巴瘤风险相关。我们在此报告一例在使用巴瑞替尼治疗期间并发重度AD的ALK阴性间变性大细胞淋巴瘤(ALK-ALCL)病例,巴瑞替尼是一种用于治疗AD的口服、选择性且可逆的 Janus激酶(JAK)1和2抑制剂。二代测序(NGS)显示TP53 p.G266E突变,提示这是该疾病的触发因素及其难治病程的原因。JAK/信号转导子和转录激活子(STAT)通路在ALCLs的肿瘤细胞中常被激活,提示其为治疗靶点。巴瑞替尼与淋巴瘤发生之间的因果关系尚不清楚;然而,该患者在巴瑞替尼治疗期间发生了伴有TP53突变的ALK-ALCL。