The p53 protein plays a central role in cellular responses, including cycle arrest and cell death in response to DNA damage. Dysfunction of this protein can induce abnormal cell growth, increased cell survival, and drug resistance. The p53 tumor suppressor gene is altered in many types of human cancer including hematological malignancies. Most of the p53 biologically significant mutations impair the ability of protein to act as a transcriptional regulator. Unlike functional p53, which is rapidly degraded after its synthesis, mutated forms tend to accumulate in the cells, thus becoming detectable by immunohistochemistry. Its has been reported that mutations of p53 gene occur with a frequency of approximately 12.5% in lymphoid malignancies. However, aggressive non-Hodgkin's lymphomas (NHL), especially Burkitt's lymphoma, show higher frequencies. Most p53 gene mutations in NHL are missense mutations, stabilising the functionally defective protein, but wild-type form of p53 protein also has a high p53 expression detected by immunohistochemistry indicating a discrepancy between gene mutation and protein detection. The aim of this work is to perform a comprehensive review of the methods used to identify gene alterations and p53 protein expression in lymphoid neoplasias in order to investigate its involvement in these neoplasias.
p53 tumor suppressor gene; p53 protein; lymphoid neoplasias
