Wu Zuoqiao, Nicoll Mary, Ingham Robert J
Department of Medical Microbiology and Immunology, Li Ka Shing Institute of Virology, University of Alberta, Edmonton, Canada.
Department of Medicine, University of Toronto, Toronto, Canada.
Exp Hematol Oncol. 2021 Jan 7;10(1):4. doi: 10.1186/s40164-020-00197-9.
Classical Hodgkin lymphoma (cHL) and anaplastic lymphoma kinase-positive, anaplastic large cell lymphoma (ALK+ ALCL) are B and T cell lymphomas respectively, which express the tumour necrosis factor receptor superfamily member, CD30. Another feature shared by cHL and ALK+ ALCL is the aberrant expression of multiple members of the activator protein-1 (AP-1) family of transcription factors which includes proteins of the Jun, Fos, ATF, and Maf subfamilies. In this review, we highlight the varied roles these proteins play in the pathobiology of these lymphomas including promoting proliferation, suppressing apoptosis, and evading the host immune response. In addition, we discuss factors contributing to the elevated expression of these transcription factors in cHL and ALK+ ALCL. Finally, we examine therapeutic strategies for these lymphomas that exploit AP-1 transcriptional targets or the signalling pathways they regulate.
经典型霍奇金淋巴瘤（cHL）和间变性淋巴瘤激酶阳性的间变性大细胞淋巴瘤（ALK+ ALCL）分别是B细胞和T细胞淋巴瘤，它们表达肿瘤坏死因子受体超家族成员CD30。cHL和ALK+ ALCL的另一个共同特征是转录因子激活蛋白-1（AP-1）家族多个成员的异常表达，该家族包括Jun、Fos、ATF和Maf亚家族的蛋白质。在本综述中，我们强调了这些蛋白质在这些淋巴瘤病理生物学中所起的多种作用，包括促进增殖、抑制凋亡和逃避宿主免疫反应。此外，我们讨论了导致cHL和ALK+ ALCL中这些转录因子表达升高的因素。最后，我们研究了针对这些淋巴瘤的治疗策略，这些策略利用AP-1转录靶点或它们所调节的信号通路。
