ALK-negative anaplastic large cell lymphoma with TP53 mutation developing during the administration of baricitinib for atopic dermatitis - A case report.

IF 0.9 Q4 HEMATOLOGY

Journal of Clinical and Experimental Hematopathology Pub Date : 2025-01-01 DOI:10.3960/jslrt.24048

Hidetsugu Kawai, Shino Iwata, Sawako Shiraiwa, Masashi Miyaoka, Daisuke Ogiya, Masako Toyosaki, Shinichiro Machida, Rikio Suzuki, Makoto Onizuka, Yoshiaki Ogawa, Naoya Nakamura, Hiroshi Kawada

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Abstract

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.

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alk阴性间变性大细胞淋巴瘤伴TP53突变在巴西替尼治疗特应性皮炎期间发生- 1例报告。

众所周知，严重特应性皮炎（AD）与淋巴瘤的风险有关。巴利替尼是一种口服、选择性、可逆的 Janus 激酶（JAK）1 和 2 抑制剂，用于治疗特应性皮炎。下一代测序（NGS）证实了TP53 p.G266E突变，这表明该突变是该病的诱因，也是其难治性病程的原因。JAK/信号转导和转录激活因子（STAT）通路经常在ALCLs的肿瘤细胞中被激活，这表明它是一个治疗靶点。巴利昔替尼与淋巴瘤发生之间的因果关系尚不清楚；但该患者在接受巴利昔替尼治疗期间出现了带有TP53突变的ALK-ALCL。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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