Department of Surgery, Fujita Health University School of Medicine, Toyoake, Aichi, 470-1192, Japan.
World J Surg. 2010 Feb;34(2):242-8. doi: 10.1007/s00268-009-0344-4.
Vascular endothelial growth factor (VEGF) is involved in tumor angiogenesis and other pathophysiological processes.
We studied the localization of VEGF in human thyroid tissues to clarify its involvement in proliferative processes in a variety of thyroid disorders. Immunohistochemical analysis using purified rabbit polyclonal anti-human VEGF or anti-human CD34 antibody and a streptavidin-biotin peroxidase complex detection system was performed on 58 tissue specimens from 53 patients with different thyroid disorders and 5 normal thyroid glands.
Vascular endothelial growth factor was not detected in normal thyroid follicular cells. However, some thyroid tumor cells expressed VEGF in the cytoplasm (papillary carcinoma, 10/18; follicular carcinoma, 1/3; medullary carcinoma, 2/2; follicular adenoma, 3/11; adenomatous goiter, 2/4). In benign follicular adenoma and adenomatous goiter, weak expression of VEGF was found in small areas of the tumor, whereas in malignant thyroid tumors, it was strongly expressed in many cells. However, VEGF was not expressed in anaplastic carcinoma, malignant lymphoma, or Graves' disease. Angiovascular cells stained with CD34 antibody in tissues from different thyroid disorders reflected statistically significant differences in papillary carcinoma, follicular adenoma, and Graves' disease compared with normal thyroids, and such cells showed a trend toward increases in medullary carcinoma and adenomatous goiter. In contrast, low vascularity was observed in anaplastic carcinoma, malignant lymphoma, and follicular carcinoma.
Because VEGF probably functions as a hypoxia-inducible angiogenic factor, overexpression of this mediator, concomitant with hypervascularity, may be induced more strongly in malignant thyroid tumors, which need more oxygen to proliferate, than in benign follicular tumors. However, neither VEGF nor CD34 was expressed in anaplastic thyroid carcinoma, which is an extremely poorly differentiated malignant tumor. CD34 but not VEGF was expressed in the hyperplastic thyroid tissues of Graves' disease composed of nontransformed cells. Thus, the expression of VEGF concomitant with CD34 is suggested to reflect both the transformation and differentiation state of malignant tumors.
血管内皮生长因子（VEGF）参与肿瘤血管生成和其他病理生理过程。
我们研究了 VEGF 在人甲状腺组织中的定位，以阐明其在各种甲状腺疾病的增殖过程中的作用。使用纯化的兔抗人 VEGF 多克隆抗体或抗人 CD34 抗体以及链霉亲和素-生物素过氧化物酶复合物检测系统，对 53 例不同甲状腺疾病患者的 58 个组织标本和 5 个正常甲状腺进行了免疫组织化学分析。
正常甲状腺滤泡细胞中未检测到 VEGF。然而，一些甲状腺肿瘤细胞在细胞质中表达 VEGF（乳头状癌，18/10；滤泡状癌，3/1；髓样癌，2/2；滤泡性腺瘤，11/3；腺瘤性甲状腺肿，4/2）。在良性滤泡性腺瘤和腺瘤性甲状腺肿中，肿瘤的小区域内 VEGF 表达较弱，而在恶性甲状腺肿瘤中，许多细胞强烈表达 VEGF。然而，VEGF 在间变性癌、恶性淋巴瘤或 Graves 病中不表达。在不同甲状腺疾病的组织中用 CD34 抗体染色的血管细胞在乳头状癌、滤泡性腺瘤和 Graves 病中与正常甲状腺相比有统计学意义的差异，并且这些细胞在髓样癌和腺瘤性甲状腺肿中呈增加趋势。相反，在间变性癌、恶性淋巴瘤和滤泡状癌中观察到低血管生成。
由于 VEGF 可能作为缺氧诱导的血管生成因子发挥作用，因此在需要更多氧气来增殖的恶性甲状腺肿瘤中，这种介质的过度表达可能伴随着更多的血管生成。然而，在极度低分化的恶性肿瘤间变性甲状腺癌中，既没有表达 VEGF，也没有表达 CD34。在 Graves 病由未转化细胞组成的增生性甲状腺组织中，表达 CD34，但不表达 VEGF。因此，VEGF 与 CD34 的共表达反映了恶性肿瘤的转化和分化状态。
