Expression of cyclin D1, retinoblastoma gene protein, and p16 MTS1 protein in atypical adenomatous hyperplasia and adenocarcinoma of the lung - An immunohistochemical analysis
Expression of cyclin D1, retinoblastoma gene protein, and p16 MTS1 protein in atypical adenomatous hyperplasia and adenocarcinoma of the lung - An immunohistochemical analysis
复制标题
DOI：
10.1007/s004280050157
复制
发表时间：
1998-03-01
期刊：
影响因子：
3.5
通讯作者：
Kitamura, H
中科院分区：
文献类型：
--
作者：
Kurasono, Y;Ito, T;Kitamura, H
为了阐明在肺腺癌（AC）发展过程中发生的导致细胞生长控制中断的事件，我们使用免疫组织化学方法评价G1周期调节因子、细胞周期蛋白D1、Rb蛋白（pRb）和p16 MTS 1蛋白以及肿瘤增殖标记物Ki 67在肺AC及其前体病变非典型腺瘤样增生（AAH）中的表达。AAH中cyclin DI过表达的病变频率相对较高（47-89%），但在早期AC（28%）和明显AC（35%）中降低。pRb表达的缺失在AAH（0-18%）和早期AC（0%）中都是罕见的，即使在显性AC中也是罕见的（13%）。在癌前病变和恶性病变中，p16表达的缺失也相对罕见（11-25%）。我们的研究结果表明，细胞周期蛋白D1的过度表达是一个早期事件，并在肺AC的肿瘤发生中起着重要的作用。然而，细胞周期蛋白D1的过度表达是不需要的恶性表型的发展和维护。这是可能的，一些细胞周期蛋白D1的非依赖性途径以外的Rb和p16异常有一个重要的作用，从AAH的恶性转化为早期AC。
To clarify the events leading to the disruption of cell growth control that occurs during the development of pulmonary adenocarcinoma (AC), we used immunohistochemistry to evaluate the expression of G1 cycle regulators, cyclin D1, Rb protein (pRb), and p16 MTS1 protein and the tumour proliferation marker, Ki 67, both in AC of the lung and in its precursor lesion, atypical adenomatous hyperplasia (AAH). The frequency of lesions with cyclin DI overexpression was relatively high in AAH (47-89%), but was decreased in early AC (28%) and overt AC (35%). The loss of pRb expression was rare in both AAH (0-18%) and early AC (0%), and was infrequent even in overt AC (13%). The loss of p16 expression was also relatively infrequent in both the premalignant and the malignant lesions (11-25%). Our results suggest that overexpression of cyclin D1 is an early event and plays an important part in tumorigenesis in the case of lung AC. However, cyclin D1 overexpression is not required for the development and maintenance of a malignant phenotype. It is likely that some cyclin D1-independent pathways other than Rb and p16 abnormalities have an important role in the malignant transformation from AAH to early AC.