The Role of bcl-2 in Lymphoid Differentiation and Neoplastic Transformation
Follicular lymphoma is one of the most common hematopoietic malignancies in the western world. Most (70–80%) of these tumors exhibit a characteristic t(14;18) chromosome translocation caused by recombination of the bcl-2 gene into the immunoglobulin (Ig) heavy chain locus [1–3]. The coding portion of bcl-2 remains unchanged but its regulation is presumably perturbed because of the influence of immunoglobulin regulatory sequences. The bcl-2 gene encodes a 26 kD non-glycosylated cytoplasmic protein [4, 5] which associates with membranes via its hydrophobic C-terminus . It has been variously reported to be associated with the plasma membrane and perinuclear endoplasmic reticulum  and with the inner membrane of the mitochondrion . The first clue to the unusual function of bcl-2 was the discovery that enforcing its expression in factor dependent cell lines enabled them to survive in the absence of growth factor . This observation raised the possibility that the normal role of bcl-2 is to govern the life and death of lymphocytes during the generation and function of the immune system. Transgenic mice have been developed to test this hypothesis and to evaluate the oncogenic potential of bcl-2 [9–13].
KeywordsFollicular Lymphoma Immune Complex Glomerulonephritis Heavy Chain Locus Composite Lymphoma Lymphoid Differentiation
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