Immunohistochemical Demonstration of Antiapoptotic Proliferating Protein Bcl-2 in the Ameloblastomas

Apoptosis, also known as programmed cell death or physiologic cell death, plays diverse roles in embryogenesis and normal homeostasis as well as in oncogenesis. Apoptotic processes are modulated by several geneencoded products, including the Bcl-2 family proteins, which have inhibitory or stimulatory effects.1 Bcl-2 derives its name from B-cell lymphoma 2, as it is the second member of a range of proteins initially described as a reciprocal gene translocation in chromosomes 14 to 18 in follicular lymphomas.4 They govern mitochondrial outer membrane permeabilization and can be either proapoptotic (Bax, BAD, Bak, and Bok, among others) or antiapoptotic (including Bcl-2 proper, Bcl-xL, and Bcl-w, among an assortment of others). There are a total of 25 genes in the Bcl-2 family known to date. The Bcl-2 gene product protects cells by blocking postmitotic differentiation from apoptosis, thus maintaining a stem cell pool.5 In the present study, the expression of the Bcl-2 protein was examined immunohistochemically (IHC) in different types of ameloblastomas to clarify the possible roles of this Bcl-2 protein in oncogenesis and cytodifferentiation of tumors derived from odontogenic epithelium.