Burkitt's lymphoma (BL) originates from a germinative centre cell that loses proliferation control due to activation of the c-myc gene. Apoptosis resistance is a major cause of chemotherapy failure in most kinds of cancers, including BL. The high rate of apoptosis seen in the early steps of genesis of BL is followed by a subsequent development of inactivation of pathways leading to cell death by apoptosis. A major pathway known to be altered in BL is the one mediated by the p53 protein. This pathway is important to control cell proliferation in response to DNA damage. Data from the literature show a correlation between TP53 gene mutations and treatment resistance. However, some studies have demonstrated that distinct types of mutations have the ability to confer different cell responses to chemotherapy. We found that BL cell lines bearing distinct mutations of p53 also present different responses to drug-induced apoptosis, when using drugs that act through this pathway, such as doxorubicin. Different types of mutations might confer distinct functional phenotypes. Loss of function does not always occur which may be considered an important component of chemotherapy resistance in BL. In this article we review publications regarding the response to treatment in BL while we discuss the role of TP53 gene mutations in chemotherapy resistance of these tumors.
Burkitt's lymphoma; TP53 gene; mutation; resistance; treatment
