HODGKINS-DISEASE, LYMPHOMATOID PAPULOSIS, AND CUTANEOUS T-CELL LYMPHOMA DERIVED FROM A COMMON T-CELL CLONE
HODGKINS-DISEASE, LYMPHOMATOID PAPULOSIS, AND CUTANEOUS T-CELL LYMPHOMA DERIVED FROM A COMMON T-CELL CLONE
复制标题
DOI：
10.1056/nejm199204233261704
复制
发表时间：
1992-04-23
影响因子：
158.5
通讯作者：
KADIN, ME
中科院分区：
文献类型：
--
作者：
DAVIS, TH;MORTON, CC;KADIN, ME
背景。 淋巴瘤样丘疹病是一种良性皮疹，10% 至 20% 的患者与淋巴瘤的发展相关。淋巴瘤样丘疹病的非典型细胞在组织学上类似于皮肤T细胞淋巴瘤的恶性细胞或霍奇金病的里德-斯滕伯格细胞。我们研究了一名 1971 年患淋巴瘤样丘疹病、1975 年患霍奇金病和 1985 年患皮肤 T 细胞淋巴瘤的患者，以确定这些疾病是否具有克隆相关性。方法。 T 细胞受体 α 链基因是从源自晚期皮肤 T 细胞淋巴瘤的细胞系中克隆并测序的，并使用聚合酶链反应在早期获得的受霍奇金病或淋巴瘤样丘疹病影响的组织中寻找 α 链基因的重排。结果。 在患者受淋巴瘤样丘疹病和霍奇金病影响的早期组织中检测到α链基因的肿瘤特异性重排，但在对照组织中未检测到，包括霍奇金病分期剖腹手术中未受累的组织。细胞遗传学研究揭示了皮肤 T 细胞淋巴瘤系和皮肤 T 细胞淋巴瘤临床发病前两年切除的皮肤病淋巴结中存在易位 t(8;9)(p22;p24)。免疫组织化学结果与淋巴瘤样丘疹病的非典型细胞、霍奇金病的Reed-Sternberg细胞和T细胞淋巴瘤的恶性细胞的活化T细胞表型一致。结论。 淋巴瘤样丘疹病、霍奇金病和皮肤 T 细胞淋巴瘤可以源自单个 T 细胞克隆。 t(8;9) 基因易位可能参与淋巴瘤样丘疹病或其进展为恶性疾病的发病机制。
Background. Lymphomatoid papulosis is a benign cutaneous eruption that in 10 to 20 percent of patients is associated with the development of lymphoma. The atypical cells of lymphomatoid papulosis histologically resemble the malignant cells of cutaneous T-cell lymphoma or the Reed-Sternberg cells of Hodgkin's disease. We studied a patient in whom lymphomatoid papulosis developed in 1971, Hodgkin's disease in 1975, and cutaneous T-cell lymphoma in 1985, to determine whether these diseases are clonally related.Methods. The T-cell-receptor alpha-chain gene was cloned and sequenced from a cell line derived from the advanced-stage cutaneous T-cell lymphoma, and the polymerase chain reaction was used to search for this rearrangement of the alpha-chain gene in tissues obtained earlier-that were affected by Hodgkin's disease or lymphomatoid papulosis.Results. The tumor-specific rearrangement of the alpha-chain gene was detected in the patient's earlier tissues affected by lymphomatoid papulosis and Hodgkin's disease, but not in control tissue, including uninvolved tissues from the staging laparotomy for Hodgkin's disease. Cytogenetic studies revealed a translocation, t(8;9)(p22;p24), in cutaneous T-cell lymphoma lines and in a dermatopathic lymph node removed two years before the clinical onset of the cutaneous T-cell lymphoma. Immunohistochemical findings were consistent with an activated T-cell phenotype for the atypical cells of lymphomatoid papulosis, the Reed-Sternberg cells of Hodgkin's disease, and the malignant cells of the T-cell lymphoma.Conclusions. Lymphomatoid papulosis, Hodgkin's disease, and cutaneous T-cell lymphoma can be derived from a single T-cell clone. A t(8;9) genetic translocation may be involved in the pathogenesis of lymphomatoid papulosis or its progression to malignant disease.