Klin Onkol 2003; 16(3): 141-144.
Summary: Inactivation of the tumor-suppressor gene TP53 represents loss of the control mechanism enabling the cell to effectively control the genome integrity and, in the case of its impairment, to inhibit transition into further phases of the cell cycle. This inactivation makes possible generation of a clone of cells with an altered genome, easily undergoing other changes potentially leading to malignant conversion. The loss of the tumor-suppressor function of TP53 may be a result of a series of events at the molecular level. Point mutations of TP53 leading to the overexpression of the mutated p53 protein represent one of the most frequent molecular alterations described in human solid tumors. One possibility to identify the TP53 pathology is direct detection of the mutation by DNA sequencing. The method of choice is, however, immunohistochemical detection of the overexpression of the protein product, i.e. p53 protein. In prostate carcinoma, mutations of the TP53 gene undoubtedly
occur, playing an important role in the tumor progression and probably participating in its transition into hormonally independent carcinoma. The data on the utilization of p53 as a biomarker have been, however, so far controversial.
