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骨原发性淋巴瘤中的核因子-κB 激活。

Nuclear factor-κB activation in primary lymphoma of bone.

机构信息

Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.

出版信息

Virchows Arch. 2013 Mar;462(3):349-54. doi: 10.1007/s00428-013-1372-x. Epub 2013 Jan 19.

DOI:10.1007/s00428-013-1372-x
PMID:23328932
Abstract

Primary lymphoma of bone is a rare type of extranodal diffuse large B-cell lymphoma with a relatively favourable outcome. Recent scientific interest has focused on elucidating the role of nuclear factor-κB pathway in lymphomagenesis and its potential significance as a therapeutic target. In nodal B-cell non-Hodgkin lymphomas, constitutive activation of nuclear factor-κB appears to be involved in tumour cell survival, notably in the non-germinal centre type of diffuse large B-cell lymphoma. We investigated nuclear factor-κB activation via the classical and alternative pathway in primary lymphoma of bone, through immunohistochemical staining for nuclear factor-κB family members on tumour tissues of 50 patients. Nine cases (18 %) showed nuclear staining for p50, and one case showed nuclear co-expression of p52. None of the cases showed nuclear staining for c-Rel. The nuclear staining of p50 suggests that in a minority of primary lymphomas of bone nuclear factor-κB is constitutively activated via the classical pathway. In contrast to other extranodal types of diffuse large B-cell lymphoma, there was a lack of nuclear co-expression of p65, which might suggest activation of a different pathway. Activation of nuclear factor-κB through the alternative pathway does not appear to be significantly involved, as only one case showed significant nuclear expression for p52. Finally, nuclear expression of p50 was neither preferentially detected in non-germinal centre type or germinal centre type primary lymphoma of bone, nor related to poor prognosis. Therefore, in contrast to nodal diffuse large B-cell lymphoma, the nuclear factor-κB pathway does not appear to be an attractive therapeutic target in primary lymphoma of bone.

摘要

原发性骨淋巴瘤是一种罕见的结外弥漫性大 B 细胞淋巴瘤,预后相对较好。最近的科学研究兴趣集中在阐明核因子-κB 通路在淋巴瘤发生中的作用及其作为治疗靶点的潜在意义。在结内 B 细胞非霍奇金淋巴瘤中,核因子-κB 的组成性激活似乎参与了肿瘤细胞的存活,特别是在非生发中心型弥漫性大 B 细胞淋巴瘤中。我们通过对 50 例患者的肿瘤组织进行核因子-κB 家族成员的免疫组织化学染色,研究了原发性骨淋巴瘤中核因子-κB 的经典和替代途径的激活。9 例(18%)显示 p50 核染色,1 例显示 p52 核共表达。没有病例显示 c-Rel 的核染色。p50 的核染色提示,在少数原发性骨淋巴瘤中,核因子-κB 通过经典途径持续激活。与其他结外弥漫性大 B 细胞淋巴瘤不同,缺乏 p65 的核共表达,这可能提示激活了不同的途径。替代途径的核因子-κB 激活似乎没有明显参与,因为只有 1 例显示 p52 有明显的核表达。最后,p50 的核表达既不是在非生发中心型或生发中心型原发性骨淋巴瘤中优先检测到的,也与预后不良无关。因此,与结内弥漫性大 B 细胞淋巴瘤不同,核因子-κB 途径似乎不是原发性骨淋巴瘤有吸引力的治疗靶点。

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