Kobierzycki Christopher, Grzegrzolka Jedrzej, Glatzel-Plucinska Natalia, Piotrowska Aleksandra, Wojnar Andrzej, Smolarz Beata, Romanowicz Hanna, Dziegiel Piotr
Division of Histology and Embryology, Department of Human Morphology and Embryology, Wroclaw Medical University, Wroclaw, Poland
Division of Histology and Embryology, Department of Human Morphology and Embryology, Wroclaw Medical University, Wroclaw, Poland.
In Vivo. 2018 Jul-Aug;32(4):731-736. doi: 10.21873/invivo.11301.
BACKGROUND/AIM: An impaired cell-cycle control and genetic material organization are crucial elements of carcinogenesis. p16 is a tumor suppressor protein which decelerates promotion of the cells from G to S phase, whereas special AT-rich sequence-binding protein 1 (SATB1) is a nuclear matrix protein that binds to specific regions of the DNA and ensures its proper organization and function. Increased levels of both markers are observed in various types of cancers. The aim of this study was to investigate the expression of p16 and SATB1 proteins in regard to expression of the Ki-67 antigen and available clinicopathological data (i.a. receptor status, staging and grading).
The study was performed on 130 samples of archived invasive ductal breast cancers. Immunohistochemical reactions were performed on freshly prepared tissue microarrays and subsequently scanned by a histologic scanner. Reactions were evaluated separately in the cytoplasm (p16c, SATB1c) and nucleus (p16n, SATB1n, Ki-67) with use of a quantification software under researcher supervision.
Expression was observed for Ki-67 in 100%, p16c in 90%, p16n in 89.2%, SATB1c in 98.5% and SATB1n in 87.7% of cancer cases. Statistical analysis showed strong positive correlations: p16c vs. p16n and SATB1c vs. SATB1n (p<0.001 for both) and weak positive correlations: p16c vs. SATB1c and p16c vs. SATB1n (p=0.008, p=0.027; respectively). Expression of p16n was stronger in G vs. G (p=0.034) while Ki-67 expression was stronger in cases with negative progesterone receptor status (p=0.011). All other analyzed associations were statistically insignificant.
A weak association between immunohistochemical expression of p16 and SATB1 indicated limited possibility of their independent usage. Further studies concerning determination of a wider panel of proteins controlling cell cycle should be considered.
背景/目的：细胞周期调控受损和遗传物质组织紊乱是致癌作用的关键因素。p16是一种肿瘤抑制蛋白，可减缓细胞从G期进入S期的进程，而富含AT序列的特异性结合蛋白1（SATB1）是一种核基质蛋白，可与DNA的特定区域结合并确保其正确的组织和功能。在各种类型的癌症中均观察到这两种标志物水平升高。本研究的目的是根据Ki-67抗原的表达以及可用的临床病理数据（如受体状态、分期和分级）来研究p16和SATB1蛋白的表达情况。
本研究对130份存档的浸润性导管癌样本进行。在新制备的组织微阵列上进行免疫组织化学反应，随后用组织扫描仪进行扫描。在研究者监督下，使用定量软件分别在细胞质（p16c、SATB1c）和细胞核（p16n、SATB1n、Ki-67）中评估反应情况。
在100%的癌症病例中观察到Ki-67表达，90%的病例中观察到p16c表达，89.2%的病例中观察到p16n表达，98.5%的病例中观察到SATB1c表达，87.7%的病例中观察到SATB1n表达。统计分析显示出强正相关性：p16c与p16n以及SATB1c与SATB1n（两者p均<0.001），以及弱正相关性：p16c与SATB1c以及p16c与SATB1n（分别为p=0.008，p=0.027）。p16n在G期与G期相比表达更强（p=0.034），而Ki-67在孕激素受体状态为阴性的病例中表达更强（p=0.011）。所有其他分析的关联均无统计学意义。
p16和SATB1免疫组织化学表达之间的弱关联表明它们独立使用的可能性有限。应考虑开展关于确定更广泛的细胞周期调控蛋白组的进一步研究。
