Loss of functional pRB is not a ubiquitous feature of B-cell malignancies

Human cancers frequently sustain genetic mutations that alter the function of their G1 cell cycle control check point. These include changes to the re tinoblastoma gene and to the genes that regulate its phosphorylation, such as the cyclin-dependent kinase inhibitor p16(INK4a). Altered expression of retinoblastoma protein (pRb) is associated with non-Hodgkin's lymphoma, par ticularly centroblastic and Burkitt's lymphomas. pRb is expressed in normal B-cells and its regulatory phosphorylation pathway is activated in respons e to a variety of stimuli. Since human B-lymphoma-derived cell lines are of ten used as in vitro model systems to analyse the downstream effects of sig nal transduction, we examined the functional status of pRb in a panel of hu man B-cell lines. We identified eleven cell lines which express the hyperph osphorylated forms of pRb. Furthermore, we suggest that the pRb protein app ears to be functional in these cell lines.