Expression profile of apoptotic mediators and proliferative markers in oral squamous cell carcinoma

Oral squamous cell carcinoma (OSCC) represents a major health problem worldwide. It is therefore essential to develop a deeper understanding of its biology. Beside the recent hypothesis of cancer stem cells, the consideration of its cell death and cell proliferation has emerged as important diagnostic and prognostic tools. PURPOSE OD THE STUDY: Detection of the proportion of cell loss monitored by apoptosis-related genes, p53, p21 and Bcl2, and their relationship to the pathological proliferation parameter, PCNA in OSCC. Furthermore, discussion of the hypothesis of cancer stem cell biology in OSCC would be anticipated.

Archival 35 tissue embedded paraffin blocks, that were previously diagnosed as well to moderately differentiated OSCC, were immunohistochemically stained using a panel of antibodies including apoptotic mediators, p53, p21, Bcl2, and proliferation marker, PCNA. Immunoexpression was scored using a semiquantitative scale and statistically analyzed.

The clinico-pathological data revealed that mean age was 46.9±8.2 and the tongue was the most affected site, followed by the palate then the floor of the mouth. There was no significant difference between metastasizing and non-metastasizing patients regarding age or gender (p=0.174, 0.404, respectively). On the other hand, variable profile patterns of the investigated indicators existed, where PCNA positively immunostaining cells was 100%while P21 recorded the higher percentage of negatively immunoreactive cells (42.9%). A common trait for the studied cell cycle indicators was that the basal and suprabasal epithelial cells as well as the peripheral cells of the invading nests were the harbor of immunoreactivity. Meanwhile, PCNA immunopositivity was revealed in all epithelial layers plus stromal cells.

Assessment of the studied cell cycle regulators may be valuable to judge tumorigenesis of OSCC. Furthermore, deregulation of cell cycle control might aid in the attainment of genetic changes in normal stem cells to be altered to cancer stem cells.