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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
Published on: December 19, 2019
ALK-negative anaplastic large cell lymphoma with TP53 mutation developing during the administration of baricitinib
Hidetsugu Kawai1, Shino Iwata1, Sawako Shiraiwa1
1Department of Hematology / Oncology, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
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.
