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NCI CANCERLIT^® Search: Retinoblastoma Gene (RB) - April 2002

National Cancer Institute^®
Last Modified: April 1, 2002

The family of retinoblastoma proteins.

Reversion of Ras transformed cells by Ets transdominant mutants.

Clinical significance of molecular genetic changes in sporadic invasive pituitary adenomas.

ARF is not required for apoptosis in Rb mutant mouse embryos.

Table of Contents

1
UI - 11693966
AU - Stiegler P; Giordano A
TI - The family of retinoblastoma proteins.
SO - Crit Rev Eukaryot Gene Expr 2001;11(1-3):59-76
AD - Department of Pathology, Anatomy and Cell Biology, Jefferson Medical College, Philadelphia, PA 19107, USA.
Our understanding of how the retinoblastoma family members, pRB/p105, pRB2/p130, and pRBL1/p107, regulate cellular properties has progressed significantly. Mechanisms have been described regarding how these proteins utilize properties of additional factors, such as histone deacetylases, to negatively regulate transcription. More importantly, the retinoblastoma proteins have been integrated within multiple cellular pathways, and a complex view has emerged on how the individual members respond to various external and internal stimuli. pRB/p105 is best described in its biochemical properties as well as in the resulting cellular functions. Less is known about pRB2/p130 and pRBL1/p107, but an improved map of their individual as well as redundant functions has been drawn over the last years. In this review we describe general aspects of the properties and functions of the three retinoblastoma family members and their protein-binding partners in cellular growth control.

2
UI - 7970725
AU - Wasylyk C; Maira SM; Sobieszczuk P; Wasylyk B
TI - Reversion of Ras transformed cells by Ets transdominant mutants.
SO - Oncogene 1994 Dec;9(12):3665-73
AD - CNRS-LGME, INSERM-U. 184, Institut de Chimie Biologique, Faculte de Medecine, Strasbourg, France.
Considerable progress has been made in elucidating the components of the Ras signalling pathway, from both biochemical and genetic investigations. However little is known about the nuclear targets of the pathway, and in particular those that mediate the long-term changes in gene expression resulting from Ras transformation. Ets family members may be involved in these processes since Ras stimulates transcription through ets-DNA binding sites. We show that a mutated Ets protein, delta PU.1, inhibits Ras activation of transcription. Stable expression of delta PU.1 in Ras transformed NIH3T3 fibroblasts reverts the transformed phenotype by many characteristics, including morphology, anchorage independent growth, saturation density, growth in low serum, tumour formation in nude mice and to some extent sensitivity to apoptotic cell death. Similar trans-dominant mutants of c-Ets-1 and c-Ets-2, the most divergent members of the Ets-family to PU.1, also revert Ras transformed cells, as indicated by morphology, anchorage-independent growth, saturation density and doubling time in low serum. Reversion may result from a shared property of the mutants, such as binding to ets motifs in promoters. These results provide evidence for an important role for Ets proteins in Ras transformation.

3
UI - 11642545
AU - Nam DH; Song SY; Park K; Kim MH; Suh YL; Lee JI; Kim JS; Hong SC; Shin
TI - HJ; Park K; Eoh W; Kim JH Clinical significance of molecular genetic changes in sporadic invasive pituitary adenomas.
SO - Exp Mol Med 2001 Sep 30;33(3):111-6
AD - Department of Neurosurgery, Samsung Medical Center and Center for Clinical Research, Sungkyunkwan University School of Medicine, Sungkyunkwan University, Seoul, Korea.
Several molecular and genetic changes have been found in pituitary adenomas. We looked for correlations between these changes and the degree of invasiveness of the tumors. The invasiveness of 11 pituitary adenomas was graded by Hardy classification. We examined the retinoblastoma gene (RB1.20 on chromosome 13q) and the region around the MEN1 locus (chromosome 11q13.1-5) for loss of heterozygosity. Also examined are p53 mutations using single strain conformation polymorphism, p53 protein overexpression using immuno cytochemistry, homozygous deletions of p15 and p16 by polymerase chain reaction, and cellular proliferative activity using MIB-1 antibody. Six tumors (54.5%) had an LOH at either RB1.20 or the MEN1 locus. LOHs were found more frequently in Grade 4 and stage E tumors (72% and 67%) than in Grade 3 and stage D tumors (25% and 40%). However, no mutation or overexpression of p53 was found. No homozygous deletions of p15 or p16 were identified. The cell proliferative index ranged from 0 to 3%. LOH at 11q13 and 13q may be valuable in predicting the invasiveness of pituitary adenomas.

4
UI - 11818069
AU - Tsai KY; MacPherson D; Rubinson DA; Crowley D; Jacks T
TI - ARF is not required for apoptosis in Rb mutant mouse embryos.
SO - Curr Biol 2002 Jan 22;12(2):159-63
AD - MIT Department of Biology and Center for Cancer Research, Cambridge, MA 02139, USA.
The retinoblastoma (RB) tumor suppressor gene occupies central roles in cell cycle control and tumor suppression. Homozygous mutant (Rb(-/-)) embryos die at E13.5-E15.5, exhibiting extensive apoptosis and inappropriate S phase entry in the central and peripheral nervous systems, liver, and ocular lens. Mice simultaneously mutant for Rb and other genes can be generated to assess the requirement for these genes in cell cycle control and apoptosis. Using such analysis, E2f-1, E2f-3, p53, and Id2 have been identified as important regulators of cell cycle control and apoptosis in Rb(-/-) embryos. Because unrestrained E2F activity in the absence of Rb function contributes to p53-dependent apoptosis in many systems, we wished to identify genes linking deregulated E2F activity to p53 activation and subsequent apoptosis. As a transcriptional target of E2F-1, a regulator of p53, and an important mediator of apoptosis, ARF was a strong candidate for such a role, especially since it can be upregulated in the absence of Rb. From the analysis of Rb/ARF compound mutants we demonstrate that ARF is not an obligatory link between Rb inactivation and p53-dependent apoptosis.

The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.

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