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Prepublished online as a Blood First Edition Paper on September 12, 2002; DOI 10.1182/blood-2002-07-2009.
Submitted July 8, 2002
Accepted September 3, 2002
Cell cycle deregulation in B-cell lymphomas
Margarita Sanchez-Beato, Abel Sanchez-Aguilera, and Miguel A Piris*
Molecular Pathology Program, Centro Nacional de Investigaciones Oncologicas (CNIO), Madrid, Spain
* Corresponding author; email: mapiris{at}cnio.es.
Disruption of the physiological balance between cell proliferation and death is a universal feature of all cancers. In general terms, human B-cell lymphomas can be subdivided into two main groups, low- and high-growth fraction lymphomas, according to the mechanisms through which this imbalance is achieved. Most types of low-growth fraction lymphomas are initiated by molecular events resulting in the inhibition of apoptosis, such as translocations affecting BCL2, in Follicular Lymphoma, or BCL10 and API2/MLT1, in MALT Lymphomas. This results in cell accumulation as a consequence of prolonged cell survival. In contrast, high-growth fraction lymphomas are characterized by an enhanced proliferative activity, as a result of the deregulation of oncogenes with cell cycle regulatory functions, such as BCL6, in Large B-Cell Lymphoma, or c-myc, in Burkitt Lymphoma. Low- and high-growth fraction lymphomas are both able to accumulate other alterations in cell cycle regulation, most frequently involving tumor suppressor genes such as p16INK4a, p53 and p27KIP1. As a consequence, these tumors behave as highly aggressive lymphomas. The simultaneous inactivation of several of these regulators confers increased aggressivity and proliferative advantage to tumoral cells. In this review, we discuss our current knowledge of the alterations in each of these pathways, with special emphasis on the deregulation of cell cycle progression, in an attempt to integrate the available information within a global model that describes the contribution of these molecular changes to the genesis and progression of B-cell lymphomas.
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