Okoń Krzysztof, Klimkowska Agnieszka, Wójcik Piotr, Osuch Czesław, Papla Bolesław, Stachura Jerzy
Department of Pathomorphology, Collegium Medicum, Jagiellonian University, Kraków.
Pol J Pathol. 2006;57(1):23-8.
The development of new blood vessels is a prerequisite for progression of malignant neoplasms. Factors that induce neoangiogenesis include VEGF, VEGF-C, VEGF-D, PD-ECG, ANG-2, TSP-1, HIF-1 and HIF-2. From the etiopathogenetic viewpoint, colorectal carcinoma is heterogenic. It may develop via a sequence of mutations leading to chromosome instability or else result from DNA repair defects, which are manifested as microsatellite instability. The objective of the present investigations was the comparison of neoangiogenesis in microsatellite-stable colorectal carcinomas, as well as in tumors with low and high instability levels. The material included 71 surgical cases of colorectal carcinoma. Vessel density was assessed by immunohistochemical reactions to CD34 and vWf, calculating the number of vessel sections within the invasion margin, in visual fields selected at random, and within hot spots. Microsatellite instability was evaluated in frozen materials employing the PCR reaction with gel and capillary electrophoresis. In all the cases, the authors detected CD34+ and less numerous vWf+ vessels within the tumor and in its vicinity. In 45 cases, no microsatellite instability was found, in 13 cases, low level instability (MSI-L) was observed, and in another 13 - high microsatellite instability (MSI-H). Some differences in vessel density were noted between the above groups, yet they were not statistically significant. On the other hand, the authors observed more numerous CD34+ vessels in cases with metastases to the regional lymph nodes. In conclusion, it is suggested that neoangiogenesis in sporadic colorectal carcinoma is directly related to metastatic potential, but not to MSI status.
新血管的形成是恶性肿瘤进展的先决条件。诱导新血管生成的因素包括血管内皮生长因子(VEGF)、VEGF - C、VEGF - D、血小板衍生内皮细胞生长因子(PD - ECG)、血管生成素 - 2(ANG - 2)、血小板反应蛋白 - 1(TSP - 1)、缺氧诱导因子 - 1(HIF - 1)和缺氧诱导因子 - 2(HIF - 2)。从病因发病学角度来看,结直肠癌具有异质性。它可能通过一系列导致染色体不稳定的突变发展而来,或者由DNA修复缺陷导致,这种缺陷表现为微卫星不稳定。本研究的目的是比较微卫星稳定的结直肠癌以及微卫星不稳定程度低和高的肿瘤中的新血管生成情况。材料包括71例结直肠癌手术病例。通过对CD34和血管性血友病因子(vWf)的免疫组化反应评估血管密度,计算侵袭边缘、随机选择的视野以及热点区域内的血管切片数量。采用凝胶和毛细管电泳的PCR反应在冷冻材料中评估微卫星不稳定情况。在所有病例中,作者在肿瘤及其附近检测到CD34 +血管,而vWf +血管数量较少。45例未发现微卫星不稳定,13例观察到低水平不稳定(微卫星低度不稳定,MSI - L),另外13例为高微卫星不稳定(微卫星高度不稳定,MSI - H)。上述组间在血管密度上存在一些差异,但无统计学意义。另一方面,作者观察到区域淋巴结转移病例中的CD34 +血管数量更多。总之,提示散发性结直肠癌中的新血管生成与转移潜能直接相关,但与微卫星不稳定状态无关。