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 retinoblastoma gene and to the genes that regulate its phosphorylation, such as the cyclin-dependent kinase inhibitor p16INK4a. Altered expression of retinoblastoma protein (pRb) is associated with non-Hodgkin's lymphoma, particularly centroblastic and Burkitt's lymphomas. pRb is expressed in normal B-cells and its regulatory phosphorylation pathway is activated in response to a variety of stimuli. Since human B-lymphoma-derived cell lines are often used as in vitro model systems to analyse the downstream effects of signal transduction, we examined the functional status of pRb in a panel of human B-cell lines. We identified eleven cell lines which express the hyperphosphorylated forms of pRb. Furthermore, we suggest that the pRb protein appears to be functional in these cell lines.
Sinclair
A J
AJ
School of Biological Sciences, University of Sussex, Brighton, E Sussex, UK.
Frost
V
V
D002051:Burkitt Lymphoma / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D002478:Cells, Cultured; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000096:biosynthesis; D015972:Gene Expression Regulation, Neoplastic; D016161:Genes, Retinoblastoma / Q000502:physiology*; D006566:Herpesviridae Infections / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D004854:Herpesvirus 4, Human; D006801:Humans; D016393:Lymphoma, B-Cell / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D010766:Phosphorylation; D016160:Retinoblastoma Protein / Q000096:biosynthesis / Q000235:genetics* / Q000502:physiology*; D014407:Tumor Cells, Cultured; D014412:Tumor Virus Infections / Q000235:genetics / Q000378:metabolism / Q000473:pathology
D019941:Cyclin-Dependent Kinase Inhibitor p16; D016160:Retinoblastoma Protein