Garewal Jessica, Garewal Ripin, Sircar Keya
Senior Lecturer, Department of Oral Pathology and Microbiology, National Dental College and Hospital , Derabassi, India .
Senior Lecturer, Department of Pedodontics and Preventive Dentistry, National Dental College and Hospital , Derabassi, India .
J Clin Diagn Res. 2014 Jul;8(7):QC01-4. doi: 10.7860/JCDR/2014/6474.4562. Epub 2014 Jul 20.
Neoplasia results from various genetic and epigenetic factors. Our study focused on the pathogenesis which involved an imbalance in various molecular mechanisms which regulated cell proliferation and apoptosis. The anti-apoptotic mechanism is regulated by Bcl-2 gene, while Ki-67 is expressed exclusively in nuclei of proliferating cells. This study was done to evaluate the basic pathologic process which underlay well and poorly differentiated oral squamous cell carcinoma (OSCC).
Thirty cases of oscc were selected, out of which 11 were well differentiated, 9 were moderately differentiated and 10 were poorly differentiated. Three slides of 4μm thickness were prepared out of each sample, which were then subjected to Hematoxylin and eosin stain (H&E) staining and two types of immunohistochemical (IHC) staining. Immunohistochmical markers used were Ki-67 (proliferative marker using MIB-1 (Molecular Immunology Borstel 1) antibody) and Bcl-2 (anti-apoptotic marker). The number of MIB-1 and Bcl-2 positive cells was calculated from ten different high power fields, by counting the number of positive cells per 50 cells in each field, by making a grid pattern. The overall percentage value for each case was evaluated for MIB-1 and Bcl-2 positive cells. Karl-Pearson's co-relation coefficient was calculated between MIB-1 and Bcl-2 in each group. The aim of this study was to co-relate the expression of Ki-67, a proliferative marker, by using MIB-1 antibody and Bcl-2, an anti-apoptotic marker in various grades of oscc and also to determine whether there was any co-relation between these two markers in the 30 cases of oscc .
A statistically significant increase for MIB-1 and a statistically significant decrease for Bcl-2 was found in well to moderately to poorly differentiated Squamous cell carcinoma (SCC). A statistically significant co-relation was also found between MIB-1 and Bcl-2 in poorly differentiated oscc .
MIB-1 expression is predominant in well, moderate and poorly differentiated SCCs. Bcl-2 expression is predominant in well differentiated than in moderately and poorly differentiated oscc , which suggested that apoptosis probably played a major role in the early stages of carcinogenesis.
肿瘤形成由多种遗传和表观遗传因素导致。我们的研究聚焦于发病机制,其涉及调节细胞增殖和凋亡的各种分子机制失衡。抗凋亡机制由Bcl-2基因调控,而Ki-67仅在增殖细胞的细胞核中表达。本研究旨在评估高分化和低分化口腔鳞状细胞癌(OSCC)的基本病理过程。
选取30例OSCC病例,其中高分化11例,中分化9例,低分化10例。每个样本制备3张4μm厚的玻片,然后进行苏木精和伊红染色(H&E)以及两种免疫组织化学(IHC)染色。使用的免疫组织化学标志物为Ki-67(使用MIB-1(分子免疫学博尔斯特尔1)抗体的增殖标志物)和Bcl-2(抗凋亡标志物)。通过在十个不同的高倍视野中计数每个视野中每50个细胞中的阳性细胞数来计算MIB-1和Bcl-2阳性细胞的数量,采用网格模式。评估每个病例中MIB-1和Bcl-2阳性细胞的总体百分比值。计算每组中MIB-1和Bcl-2之间的Karl-Pearson相关系数。本研究的目的是通过使用MIB-1抗体和抗凋亡标志物Bcl-2来关联增殖标志物Ki-67在不同分级的OSCC中的表达,并确定这两种标志物在30例OSCC病例中是否存在任何相关性。
在高分化至中分化至低分化鳞状细胞癌(SCC)中,发现MIB-1有统计学意义的增加,Bcl-2有统计学意义的减少。在低分化OSCC中,MIB-1和Bcl-2之间也发现有统计学意义的相关性。
MIB-1表达在高分化、中分化和低分化SCC中占主导。Bcl-2表达在高分化OSCC中比在中分化和低分化OSCC中占主导,这表明凋亡可能在致癌作用的早期阶段起主要作用。