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

Imprima English

National Cancer Institute^®
Ultima Vez Modificado: 1 de septiembre del 2002

Multiple centrosomes arise from tetraploidy checkpoint failure and mitotic centrosome clusters in p53 and RB pocket protein-compromised
Chromosomal aberrations are shared by malignant plasma cells and a small fraction of circulating CD19+ cells in patients with myeloma and
Significance of loss of heterozygosity of the RB1 gene during tumour progression in well-differentiated liposarcomas.

Table of Contents

1
UI - 12119403
AU - Borel F; Lohez OD; Lacroix FB; Margolis RL
TI - Multiple centrosomes arise from tetraploidy checkpoint failure and mitotic centrosome clusters in p53 and RB pocket protein-compromised cells.
SO - Proc Natl Acad Sci U S A 2002 Jul 23;99(15):9819-24
AD - Institut de Biologie Structurale Jean-Pierre Ebel, Commissariat a l'Energie Atomique-Centre National de la Recherche Scientifique, 41 Rue Jules Horowitz, 38027 Grenoble Cedex 1, France.
A high degree of aneuploidy characterizes the majority of human tumors. Aneuploid status can arise through mitotic or cleavage failure coupled with failure of tetraploid G(1) checkpoint control, or through deregulation of centrosome number, thus altering the number of mitotic spindle poles. p53 and the RB pocket proteins are important to the control of G(1) progression, and p53 has previously been suggested as important to the control of centrosome duplication. We demonstrate here that neither suppression of p53 nor of the RB pocket protein family directly generates altered centrosome numbers in any of several mammalian primary cell lines. Instead, amplification of centrosome number occurs in two steps. The first step is failure to arrest at a G(1) tetraploidy checkpoint after failure to segregate the genome in mitosis, and the second step is clustering of centrosomes at a single spindle pole in subsequent tetraploid or aneuploid mitosis. The trigger for these events is mitotic or cleavage failure that is independent of p53 or RB status. Finally, we find that mouse embryo fibroblasts spontaneously enter tetraploid G(1), explaining the previous demonstration of centrosome amplification by p53 abrogation alone in these cells.

2
UI - 12060120
AU - Zojer N; Schuster-Kolbe J; Assmann I; Ackermann J; Strasser K; Hubl W;
TI - Drach J; Ludwig H Chromosomal aberrations are shared by malignant plasma cells and a small fraction of circulating CD19+ cells in patients with myeloma and monoclonal gammopathy of undetermined significance.
SO - Br J Haematol 2002 Jun;117(4):852-9
AD - First Department of Internal Medicine and Medical Oncology, Wilhelminenspital, University of Vienna, Montleartstrasse 37, 1160 Vienna, Austria.
In the present study, we aimed to identify distinct structural and numerical chromosomal aberrations in peripheral blood B cells of patients with myeloma and monoclonal gammopathy of undetermined significance (MGUS), which reflect changes thought to occur at different stages of the disease process. Peripheral blood from 12 patients with multiple myeloma and three patients with MGUS was investigated for the occurrence of retinoblastoma-1 gene deletions, p53 gene deletions and numerical aberrations demonstrated previously to be present in the patients' bone marrow CD138+ cells. By combining immunocytochemical staining for light chains and interphase fluorescence in situ hybridization (FISH), aberrant light-chain +ve cells were detected in the circulating CD19+ cell fraction. Each kind of chromosomal change present in the myeloma tumour cells was found to be shared by a small fraction of CD19+ cells (0.1-1.8%; median 0.36%, n = 6). In one MGUS patient, aberrant cells could be identified with a frequency of 0.34% within the CD19-sorted cell fraction. Clonotypic cells were detected with a frequency of 0.01-0.07% of peripheral blood nucleated cells by m-RNA in situ hybridization with patient-specific probes in three investigated patients. These results provide evidence that the circulating clonotypic B cells are closely related to the malignant plasma cells in myeloma and MGUS.

3
UI - 12210086
AU - Schneider-Stock R; Boltze C; Jaeger V; Stumm M; Seiler C; Rys J; Schutze
TI - K; Roessner A Significance of loss of heterozygosity of the RB1 gene during tumour progression in well-differentiated liposarcomas.
SO - J Pathol 2002 Aug;197(5):654-60
AD - Department of Pathology, Otto-von-Guericke University, 39120 Magdeburg, Leipziger Strasse 44, Germany. regine.schneider-stock@medizin.uni-magdeburg.de
Tumour progression can be investigated in liposarcomas showing a transition from a low-grade well-differentiated (WD) to a high-grade dedifferentiated (DD) variant. As RB1 gene alterations are common defects in sarcomas, this study examined the frequency of RB1 loss of heterozygosity (LOH) in a group of 14 well-differentiated liposarcomas (WDLs) and 17 well-differentiated/dedifferentiated liposarcomas (WD/DDLs), using a microdissection approach (PALM laser pressure catapulting) that allows the two histological components to be separated for polymerase chain reaction (PCR) analysis. In addition, RB1 protein expression and the Mib1 proliferation index were determined by immunohistochemistry and interphase FISH was performed with an RB1 probe at 13q14. By the use of four intragenic polymorphic RB1 markers (introns 1, 17, 20, and 25) for PCR, allelic losses were found only in the DD parts, but never in the pure WDLs or in the WD components of the WD/DDLs investigated. Furthermore, DD areas characterized by a heterogeneous RB1 protein expression pattern (35-65% immunopositivity), as compared with 90-100% RB1 positivity in WD areas, showed a marked increase in Mib1 proliferation index (19.6% versus 1.8% in WD areas; p<0.001). Interphase fluorescence in situ hybridization (FISH) detected a higher RB1-LOH rate in the DD components of WD/DDLs. Considering the different detection sensitivities of the three methodologies, it is concluded that loss of RB1 function already begins in the WDL, and that the tumour cell population with RB1-LOH starts prevailing in the tumour mass during progression of a WDL. Copyright 2002 John Wiley & Sons, Ltd.

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