P53: Revealing the Unusual Suspect: a Study and Field Cancerization Minireview.

Abstract

Oral carcinogenesis is a multistep process in which clinically recognizable prestages (leukoplakia and erythroplakia) occasionally occur [1]. Head and neck squamous cell cancer (HNSCC) is often associated with widespread epithelial histopathological alterations and despite successful treatment of a primary head and neck cancer, there is a high likelihood of occurrence of a second primary tumor similarly as seen in cases of upper aerodigestive tract and lung cancers [2]. These observations led Slaughter et at [3] to propose the concept of “field cancerization”; the hypothesis that there are carcinogen-induced changes throughout the mucosa of the upper aerodigestive tract of head and neck cancer patients. Originally, it was thought that all second primary tumors develop independently after widespread epithelial exposure to carcinogens [3]. In contrast, several other reports suggested that at least a proportion of second primary tumors in HNSCC patients have arisen from one clonal cell population which is excepted presently [4, 5]. Various mechanisms have been proposed to explain this proposed common clonal origin of second primary tumors such as shedding of premalignant cells into the saliva and implantation at other sites [4, 6] or lateral migration of isolated premalignant cells [4, 5]. Braakhuis et al. [7] proposed the patch field carcinoma model to explain progression of genetically altered stem cell to carcinoma in normal oral mucosa. This genetically altered clone of cell expands laterally even greater than 7 cm in diameter [7]. With further more genetic hits in the predisposed area malignant transformation might happen at different areas of hits, which explain the concept of second primary tumor. Accumulation of mutations in oncogenes and tumor suppressor genes is a major genetic molecular mechanism of tumor development. Among the tumor suppressor genes, inactivation of the p53 gene is one of the most frequent events [8]. Thus the aim of the present study was to evaluate the concept of field cancerization using p53 as a marker of field change in a case of patient who presented with multiple lesions ranging from premalignancy to malignant oral squamous cell carcinoma.