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心脏黏液瘤的组织发生。19例免疫组织化学研究,包括1例具有腺性结构的病例,并复习文献。

Histogenesis of cardiac myxomas. An immunohistochemical study of 19 cases, including one with glandular structures, and review of the literature.

作者信息

Johansson L

机构信息

Department of Pathology, University Hospital, Lund, Sweden.

出版信息

Arch Pathol Lab Med. 1989 Jul;113(7):735-41.

PMID:2472783
Abstract

To elucidate the histogenesis of cardiac myxomas, the literature has been reviewed, including all previous immunohistochemical studies, and an extensive immunohistochemical study of 19 cardiac myxomas has been undertaken with antibodies to factor VIII, desmin, vimentin, myoglobin, cytokeratin (CAM 5.2 and AE1/AE3), and S100 protein. In all cases, vimentin stained endothelial as well as "myxoma" (stromal) cells. In contrast, factor VIII only stained endothelial cells. In 16 cases, desmin stained cells in the vascular structures; in 5 cases, desmin stained myxoma cells. In 6 cases, S100 protein stained the myxoma cells strongly. Myoglobin was absent in all cases. In 1 case, CAM 5.2 and AE1/AE3 stained glandular structures. The results indicate the following: that most cardiac myxomas are true neoplasms derived from "embryonal rests"; that the various mesenchymal cells found in cardiac myxomas (myxoma cells, endothelial cells, smooth-muscle cells, fibroblasts, myofibroblasts, and chondroid cells), express differentiation, not histogenesis; that, apparently, only the myxoma cells are neoplastic; and that the glandular structures infrequently found in cardiac myxomas originate from entrapped foregut rests.

摘要

为阐明心脏黏液瘤的组织发生,我们查阅了相关文献,包括之前所有的免疫组织化学研究,并采用抗因子VIII、结蛋白、波形蛋白、肌红蛋白、细胞角蛋白(CAM 5.2和AE1/AE3)以及S100蛋白的抗体,对19例心脏黏液瘤进行了广泛的免疫组织化学研究。在所有病例中,波形蛋白可使内皮细胞以及“黏液瘤”(间质)细胞着色。相比之下,因子VIII仅使内皮细胞着色。16例中,结蛋白使血管结构中的细胞着色;5例中,结蛋白使黏液瘤细胞着色。6例中,S100蛋白强烈使黏液瘤细胞着色。所有病例中均未检测到肌红蛋白。1例中,CAM 5.2和AE1/AE3使腺管结构着色。结果表明:大多数心脏黏液瘤是源自“胚胎残留”的真性肿瘤;心脏黏液瘤中发现的各种间充质细胞(黏液瘤细胞、内皮细胞、平滑肌细胞、成纤维细胞、肌成纤维细胞和软骨样细胞)表现出分化,而非组织发生;显然,只有黏液瘤细胞是肿瘤性的;心脏黏液瘤中偶尔发现的腺管结构源自陷入的前肠残留。

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