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.