Segiet Oliwia Anna, Michalski Marek, Brzozowa-Zasada Marlena, Piecuch Adam, Żaba Małgorzata, Helewski Krzysztof, Gabriel Andrzej, Wojnicz Romuald
Department of Histology and Embryology, School of Medicine with the Division of Dentistry, Medical University of Silesia, Zabrze, Poland.
Department of Histology and Embryology, School of Medicine with the Division of Dentistry, Medical University of Silesia, Zabrze, Poland.
Ann Diagn Pathol. 2015 Apr;19(2):91-8. doi: 10.1016/j.anndiagpath.2015.01.002. Epub 2015 Jan 15.
Angiogenesis can be described as a formation of new vessels from the existing microvasculature and is a process of great importance to the tumor development. Parathyroid tissue can trigger spontaneous induction of angiogenesis in vitro and in vivo models in a vascular endothelial growth factor (VEGF)-dependent manner. Autotransplantated parathyroid tissue after thyroidectomy is able to form new vasculature and produce parathormone, maintaining calcium homeostasis. A great amount of factors contributes to the process of new vessel formation in primary hyperparathyroidism, such as VEGF, transforming growth factor β, and angiopoietins. Studies demonstrated that markers for angiogenesis can be useful in distinguishing between parathyroid hyperplasia and neoplasia, due to the increased angiogenesis in parathyroid proliferative lesions compared with parathyroid adenomas. These factors include, inter alia, VEGF, VEGFR2, CD105, and fibroblast growth factor-2. Although these differences appear promising in the differential diagnosis, there is an overlap between benign and malignant parathyroid lesions and there is no definite cutoff value. Loss of heterozygosity and comparative genomic hybridization studies revealed chromosomal regions frequently altered in parathyroid tumorigenesis at 9p21, 1p21-22, 1p35-36, and 11q13. Therefore, immunohistochemistry and genetic testing should be an additional diagnostic marker in combination with the traditional criteria. A better understanding of angiogenesis in primary hyperparathyroidism could result in more precise assessment of diagnosis and more effective treatment, especially in those cases, in which the commonly used parameters are insufficient.
血管生成可被描述为从现有微脉管系统形成新血管的过程，是肿瘤发展过程中极为重要的一环。甲状旁腺组织能够在体外和体内模型中以血管内皮生长因子（VEGF）依赖的方式触发血管生成的自发诱导。甲状腺切除术后自体移植的甲状旁腺组织能够形成新的脉管系统并产生甲状旁腺激素，维持钙稳态。大量因素促成了原发性甲状旁腺功能亢进中新生血管形成的过程，如VEGF、转化生长因子β和血管生成素。研究表明，血管生成标志物可用于区分甲状旁腺增生和肿瘤形成，因为与甲状旁腺腺瘤相比，甲状旁腺增殖性病变中的血管生成增加。这些因素尤其包括VEGF、VEGFR2、CD105和成纤维细胞生长因子-2。尽管这些差异在鉴别诊断中看起来很有前景，但良性和恶性甲状旁腺病变之间存在重叠，且没有明确的临界值。杂合性缺失和比较基因组杂交研究揭示了在甲状旁腺肿瘤发生过程中9p21、1p21-22、1p35-36和11q13等染色体区域经常发生改变。因此，免疫组织化学和基因检测应作为与传统标准相结合的额外诊断标志物。更好地了解原发性甲状旁腺功能亢进中的血管生成，可能会更精确地评估诊断并进行更有效的治疗，特别是在那些常用参数不足的病例中。
