Molecular analysis of oral squamous cell carcinoma: A tissue microarray study

Abstract

Bcl-2 was the most frequently expressed biomarker. The expression of Bcl-2 was inversely related to the degree of differentiation (P = 0.005). The follow-up data showed that 63.6% of the cases that were positive for both Bcl-2 and E-cadherin were disease-free following treatment. Tissue microarray technology is a promising way to analyse multiple biomarkers simultaneously. The molecular data obtained from TMA will enhance diagnosis, provide better prognostication and will improve cancer treatment for individual patients.

Expression of Bcl-2 and MIB-1 Markers in Oral Squamous Cell Carcinoma (OSCC)- A Comparative Study

“…However, in contrast to these findings, study done by Solomon et al, [14] showed an inverse relationship between Bcl-2 and levels of differentiation of OSCCs. Authors justified these findings, as there was over-expression of Bcl-2 and loss of function of p53, which played important roles in tumourigenesis of oral cancers, as they resulted in defective apoptosis and in subsequent progression of tumour.…”

KAI-1 and p53 expression in odontogenic cysts: An immunohistochemical (IHC) marker study

“…The expression of KAI-1 has been seen to decrease in cancer cell lines with high propensity for metastasis. [9][10][11][12] Cancer cells expressing KAI-1 attach to vascular endothelial cells through direct interaction between KAI-1 and DAR (an endothelial cell surface protein), leading to inhibition of tumour cell proliferation and induction of positivity. Our results are in partial agreement with their study as KAI-1 expression in dentigerous and radicular cysts were nearly comparable with their studies although OKCs exhibited KAI-1 positivity to a lesser extent.…”

“…[11] At present, a number of oncogenes and tumour suppressor genes, including p53, RAS, β-catenin and PTEN, have been implicated in various cancers. [12,13] p53 protein is a product of the tumour suppressor gene p53, which functions in the G1-S phase of the cell cycle to allow repair of the damaged DNA and to prevent the cell from entering the S phase or, alternatively, to guide the damaged cells to apoptosis. [14][15][16][17][18] Also, the high recurrence rate and clinically aggressive behaviour of OKCs have made several investigators study its cause, and the expressions of KAI-1 and p53 protein in OKCs have remained one of the most sought topics in this regard, assuming it to be associated with cell proliferation in OKCs.…”

Genome‐wide approaches (GWA) in oral and craniofacial diseases research

“…Using in vitro cell lines, carcinoembryonic antigen‐related cell adhesion molecule 1 was identified to contribute to cancer progression and result in poor prognosis (Shinozuka et al , 2009). Gene expression profiles from different types of oral cancers (Jung et al , 2010; Lunde et al , 2010; Rao et al , 2010; Solomon et al , 2010; Zhang et al , 2010a; Kim et al , 2011; Michael et al , 2011; Shao et al , 2011; Song et al , 2011) as well as from different phenotypes of the same cancers (e.g., invasiveness, response to treatment, or prognosis) have been investigated (Waseem et al , 2010; Yamazaki et al , 2010; Kang et al , 2011; Mougeot et al , 2011), as well as in different tissues (e.g., biopsy, peripheral blood). Multiple miRNAs have been reported in association with squamous cell carcinoma (Li et al , 2009; Yu et al , 2010; Scapoli et al , 2011) and adenoma (Zhang et al , 2009).…”