Sinclair, A J and Frost, V (1999) Loss of functional pRB is not a ubiquitous feature of B-cell malignancies. British Journal of Cancer, 80. pp. 670-675. ISSN 0007-0920

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Abstract

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 p16(INK4a). 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.

Item Type:	Article
Keywords:	Burkitt Lymphoma Cells, Cultured Cyclin-Dependent Kinase Inhibitor p16 Gene Expression Regulation, Neoplastic Genes, Retinoblastoma Herpesviridae Infections Herpesvirus 4, Human Humans Lymphoma, B-Cell Phosphorylation Retinoblastoma Protein Tumor Cells, Cultured Tumor Virus Infections
Schools and Departments:	School of Life Sciences > Biochemistry
SWORD Depositor:	Mx Elements Account
Depositing User:	Mx Elements Account
Date Deposited:	01 May 2020 07:20
Last Modified:	01 May 2020 07:30
URI:	http://sro.sussex.ac.uk/id/eprint/91123

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