De novo CD5+ diffuse large B-cell lymphoma:: a clinicopathologic study of 109 patients

De novo CD5+ diffuse large B-cell lymphoma:: a clinicopathologic study of 109 patients
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DOI:
10.1182/blood.v99.3.815
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发表时间:
2002-02-01
期刊:
影响因子:
20.3
通讯作者:
Nakamura, S
Nakamura, S
中科院分区:
医学1区
文献类型:
--
作者:
Yamaguchi, M;Seto, M;Nakamura, S

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已知新发 CD5(+) 弥漫性大 B 细胞淋巴瘤 (CD5(+) DLBCL) 与 CD5(-) DLBCL 和套细胞淋巴瘤 (MCL) 具有不同的表型和基因型特征。为了进一步表征CD5(+)DLBCL,对109例CD5(+)DLBCL患者进行了回顾,并将结果与​​384例CD5(-)DLBCL和128例细胞周期蛋白D1(+)MCL患者的结果进行了比较。与 CD5(-) DLBCL 患者相比,CD5(+) DLBCL 患者的年龄分布较高(中位数为 66 岁;P = .0083),女性占主导地位(男女比例为 49:60,P = .011)。与 CD5(-) DLBCL 相比,CD5(+) DLBCL 与许多侵袭性临床特征或参数的相关性更密切:69% 的患者年龄超过 60 岁 (P = .039),34% 的患者体力状态大于 1 (P = .0016),69% 的患者血清乳酸脱氢酶水平高于正常值 (P < .0001),62% 的患者在诊断时患有 III/IV 期疾病 (P = .0016)。 .0023),35% 有超过一个结外部位(P = .023),40% 有 B 症状(P = .0031)。因此,CD5(+) DLBCL 患者的总体国际预后指数评分显着高于 CD5(-) DLBCL 患者 (P = .00005)。最常见的结外受累部位是骨髓 (28%),频率高于 CD5(-) DLBCL (P < .0001),但低于细胞周期蛋白 D1(+) MCL (P = .0015)。组织病理学上,除3例免疫母细胞疾病患者外,CD5(+)DLBCL均呈中心母细胞形态,观察到滤泡间生长模式(7%)和血管内或窦内浸润(19%)。免疫表型上,CD5(+) DLBCL 的特征为 CD5(+)CD10(-)CD19(+) CD20(+)CD21(-)CD23(-) 细胞周期蛋白 D1(-) 表型和表面 IgMkappa 占优势。特别令人感兴趣的是,CD5(+) DLBCL 的生存曲线明显低于 CD5(-) DLBCL 患者 (P = .0026)。这些发现表明CD5(+) DLBCL可能构成DLBCL的一个独特亚组。 (C) 2002 年,美国血液学会。
De novo CD5(+) diffuse large B-cell lymphoma (CD5(+) DLBCL) Is known to have phenotypically and genotypically different characteristics than CD5(-) DLBCL and mantle cell lymphoma (MCL). To further characterize CD5(+) DLBCL, 109 patients with CD5(+) DLBCL were reviewed, and the results were compared with those of 384 CD5(-) DLBCL and 128 cyclin D1(+) MCL patients. Patients with CD5(+) DLBCL showed a higher age distribution (median, 66 years; P = .0083) and a female predominance (male female ratio, 49:60, P = .011) compared with those with CD5(-) DLBCL. CD5(+) DLBCL was more closely associated with many aggressive clinical features or parameters than CD5(-) DLBCL: 69% older than 60 years (P = .039), 34% with performance status greater than 1 (P = .0016), 69% with serum lactate dehydrogenase level higher than normal (P < .0001), 62% with stage III/IV disease at diagnosis (P = .0023), 35% with more than one extranodal site (P = .023), and 40% with B symptoms (P = .0031). The overall International Prognostic Index score was thus significantly higher for the patients with CD5(+) DLBCL than for those with CD5(-) DLBCL (P = .00005). The most frequent site of extranodal involvement was bone marrow (28%), a higher frequency than that for CD5(-) DLBCL (P < .0001) but lower than that for cyclin D1(+) MCL (P = .0015). Histopathologically, CD5(+) DLBCL showed centroblastic morphology except for 3 patients with immunoblastic disease, and interfollicular growth pattern (7%) and intravascular or intrasinusoidal infiltration (19%) were observed. Immunophenotypically, CD5(+) DLBCL was characterized by a CD5(+)CD10(-)CD19(+) CD20(+)CD21(-)CD23(-) cyclin D1(-) phenotype and a predominance of surface IgMkappa. Of particular interest is that CD5(+) DLBCL was characterized by a survival curve significantly inferior to that for patients with CD5(-) DLBCL (P = .0026). These findings suggest that CD5(+) DLBCL may constitute a unique subgroup of DLBCL. (C) 2002 by The American Society of Hematology.