American Society of Hematology

Fig. 7.

$Fig. 7. Lymphoma genesis and progression. / In most low-growth fraction lymphomas, cell accumulation is achieved through the inhibition of apoptosis. In contrast, in high-growth fraction BCL, proliferation is stimulated through the deregulated action of cell cycle regulators such as BCL6 or c-Myc. A fraction of both low- and high-growth fraction lymphomas acquire additional alterations affecting the tumor suppressor pathways represented by p16INK4a-cyclin D-CDK4-Rb, p14ARF-MDM2-p53-p21CIP1, and p27KIP1-cyclin E-CDK2. As a consequence, tumoral cells can bypass the multiple mechanisms by which cell cycle progression is negatively regulated in normal cells.$

Lymphoma genesis and progression.

In most low-growth fraction lymphomas, cell accumulation is achieved through the inhibition of apoptosis. In contrast, in high-growth fraction BCL, proliferation is stimulated through the deregulated action of cell cycle regulators such as BCL6 or c-Myc. A fraction of both low- and high-growth fraction lymphomas acquire additional alterations affecting the tumor suppressor pathways represented by p16^INK4a-cyclin D-CDK4-Rb, p14^ARF-MDM2-p53-p21^CIP1, and p27^KIP1-cyclin E-CDK2. As a consequence, tumoral cells can bypass the multiple mechanisms by which cell cycle progression is negatively regulated in normal cells.

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