Retinoblastoma protein (pRB) is functionally inactivated in a large number of tumors including retinoblastoma,
osteosarcoma, small-cell lung carcinoma, as well as bladder, breast and prostate cancers. The best known role of pRB in
preventing cancer is inhibition of cell cycle progression by controlling the exit from the cell cycle into G0/G1. In addition,
increasing evidence has suggested that pRB has important roles in DNA replication during S phase and G2/M transition.
The tumor suppressor function of pRB has also been demonstrated by directly promoting differentiation via cell cycle exit
with specific gene expression. Inactivation of pRB function during these cell cycle phases leads to dysregulated cell proliferation
and/or chromosomal instability, which are strongly linked to cancer development. Thus pRB plays important
roles through multiple functions in determining cell fate, i.e., normal growth/death and differentiation, or tumor formation.
Therapeutic intervention by reactivation of pRB function would be expected to be an effective treatment against various
Keywords: Cancer, cell cycle, cyclin dependent kinase, E2F, inactivation, retinoblastoma protein, Cancer, cell cycle, cyclin dependent kinase, E2F, inactivation, retinoblastoma protein, G1-S Regulator, DNA replication, gene expression, pRB
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