Retinoblastoma Tumor Suppressor Protein Expression
Published by Anonymous on 2007/9/28 (2408 reads)
1: Oncogene. 2006 Aug 28;25(38):5309-14.
Retinoblastoma gene family expression in lymphoid tissues.
Leoncini L, Bellan C, De Falco G.
Department of Human Pathology and Oncology, University of Siena, Siena, Italy. leoncinil@unisi.it
It appears more and more clear that retinoblastoma (RB) family of proteins represents key molecules in tumour suppression. This family consists of pRb/p105, p107 and pRb2/p130, which participate in a gene regulatory network that governs the cellular response to antimitogenic signals, and whose deregulation constitutes one of the hallmarks of cancer. Irrespective of their structural and biochemical similarities, RB proteins carry out different functional tasks. The expression of RB gene family in the reactive lymphoid tissues again confirms the different role of each member in cell cycle control and differentiation of normal cells. These different functional properties appear to be maintained in tumours lymphoid tissues, where alterations of the RB/p105 gene appear to be relatively rare. In this review, we will summarize the current knowledge about the role of the RB proteins in reactive and neoplastic lymphoid tissue.
Publication Types:
Review
PMID: 16936752 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
2: Leuk Lymphoma. 1998 Jan;28(3-4):275-83.
Expression of the retinoblastoma tumor suppressor gene (RB-1) in acute leukemia.
Sauerbrey A, Stammler G, Zintl F, Volm M.
University of Jena, Department of Pediatrics, Germany.
In this report we review current studies concerning the RB-1 gene expression in acute leukemias. The RB-1 gene was analyzed in several studies by protein-, RNA and DNA-techniques in acute lymphoblastic leukemia (ALL) as well as in acute myelogenous leukemia (AML). The frequency of RB-1 inactivation in ALL-patients ranged between 30% and 64% in several studies. Structural abnormalities of the RB-1 gene were reported in 18% of ALL-patients and in 27% of Philadelphia chromosome-positive ALL, respectively. The proportion of AML-patients with absent RB-1 protein expression ranged between 19% and 55%. Structural RB-1-abnormalities in AML were predominantly reported in leukemias with monocytic differentiation. Furthermore, the prognostic value of an abnormal RB-1 gene expression was also estimated in some studies. In childhood ALL RB-1 inactivation was reported to have prognostic significance while in contrast, in another study on adults no prognostic value of RB-1 was found. In 4 out of 5 documented studies AML-patients with RB-1 inactivation generally had a poorer prognosis. In conclusion, RB-1 inactivation is frequently observed in acute leukemia. The prognostic value of low RB-1 expression is controversial but the majority of published studies found low RB-1 expression to be a negative prognostic predictor, in acute leukemia.
Publication Types:
Review
PMID: 9517499 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
3: Leuk Lymphoma. 1995 Jun;18(1-2):61-7.
Abnormalities of retinoblastoma gene expression in hematological malignancies.
Zhu YM, Haynes AP, Keith FJ, Russell NH.
Department of Haematology, Nottingham City Hospital, U.K.
The human retinoblastoma gene product which is involved in cell cycle control and also acts as a transcriptional repressor of genes involved in growth control, is constitutively expressed as a phosphoprotein in normal hemopoietic cells. Abnormalities of the retinoblastoma gene expression leading to loss of protein expression either due to structural changes, mutations or transcriptional abnormalities have been found in a variety of hematological malignancies. There is evidence that loss of Rb protein expression is particularly associated with tumour progression and an adverse response to therapy which may be linked to the biological effect of Rb protein loss on the growth characteristics of tumour cells.
Publication Types:
Review
PMID: 8580830 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
4: Am J Pathol. 1992 Aug;141(2):363-75.
Expression of developmentally defined retinal phenotypes in the histogenesis of retinoblastoma.
Gonzalez-Fernandez F, Lopes MB, Garcia-Fernandez JM, Foster RG, De Grip WJ, Rosemberg S, Newman SA, VandenBerg SR.
Department of Pathology (Neuropathology), University of Virginia Health Sciences Center, Charlottesville 22908.
Retinoblastoma, the most common intraocular tumor of childhood, is a malignant neoplasm that arises during retinal development. The embryonal cell target for neoplastic transformation is not yet clearly defined. To better understand the histogenetic potential of this tumor, the expression of photoreceptor and glial cell-associated proteins were examined in 22 primary retinoblastomas. Interphotoreceptor retinol-binding protein (IRBP), cone and rod opsins were selected as the photoreceptor specific proteins due to their different temporal patterns of expression during normal retinal development. Neoplastic Müller cell differentiation, and non-neoplastic reactive astrocytes were identified using cellular retinaldehyde binding-protein (CRAlBP), and glial fibrillary acidic protein (GFAP), respectively. Photoreceptor proteins were present in 16 cases and showed different cellular patterns of expression. IRBP and cone opsin were usually abundant. Although rod opsin was clearly identified in eight tumors, its expression was more restricted than either IRBP or cone opsin. This differential pattern of expression, opposite to the normal pattern of photoreceptor gene expression in the adult retina, corresponded to a marked decrease in mRNA for rod opsin. Cone opsin and IRBP colocalized in fleurettes demonstrating that neoplastic human cone cells are capable of IRBP synthesis. Müller cell differentiation was present in 12 of the 16 cases in which photoreceptor proteins were detected. In contrast, GFAP was only present in reactive, stromal astrocytes associated with blood vessels. Our data suggest that the retinoblastoma has the histogenetic potential of the immature neural retinal epithelium which can give rise to both photoreceptor and Müller cell lineages. The differential expression of cone and rod phenotypes in retinoblastoma is consistent with the "default" mechanism of cone cell differentiation.
Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review
PMID: 1386715 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
5: Ophthalmic Paediatr Genet. 1987 Mar;8(1):3-10.
Retinoblastoma, chromosome abnormalities and oncogene expression.
Gilbert F, Potluri VR, Short MP, Kau CL, Lalatta F.
Recurrent chromosomal abnormalities in retinoblastomas involve numbers 13, 1, and 6, as well as homogeneously staining regions (HSR) and double minutes (DMS). Evidence suggesting that chromosome 13 contains a gene responsible for tumorigenesis has already been presented. We postulate that the genetic changes resulting from abnormalities of chromosomes 1 and 6 and the HSR/DMS provide a selective growth advantage to cells in which they occur. Support for this hypothesis, as it relates to the HSR/DMS and oncogene amplification, is discussed.
Publication Types:
Review
PMID: 3295640 [PubMed - indexed for MEDLINE]
Retinoblastoma gene family expression in lymphoid tissues.
Leoncini L, Bellan C, De Falco G.
Department of Human Pathology and Oncology, University of Siena, Siena, Italy. leoncinil@unisi.it
It appears more and more clear that retinoblastoma (RB) family of proteins represents key molecules in tumour suppression. This family consists of pRb/p105, p107 and pRb2/p130, which participate in a gene regulatory network that governs the cellular response to antimitogenic signals, and whose deregulation constitutes one of the hallmarks of cancer. Irrespective of their structural and biochemical similarities, RB proteins carry out different functional tasks. The expression of RB gene family in the reactive lymphoid tissues again confirms the different role of each member in cell cycle control and differentiation of normal cells. These different functional properties appear to be maintained in tumours lymphoid tissues, where alterations of the RB/p105 gene appear to be relatively rare. In this review, we will summarize the current knowledge about the role of the RB proteins in reactive and neoplastic lymphoid tissue.
Publication Types:
Review
PMID: 16936752 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
2: Leuk Lymphoma. 1998 Jan;28(3-4):275-83.
Expression of the retinoblastoma tumor suppressor gene (RB-1) in acute leukemia.
Sauerbrey A, Stammler G, Zintl F, Volm M.
University of Jena, Department of Pediatrics, Germany.
In this report we review current studies concerning the RB-1 gene expression in acute leukemias. The RB-1 gene was analyzed in several studies by protein-, RNA and DNA-techniques in acute lymphoblastic leukemia (ALL) as well as in acute myelogenous leukemia (AML). The frequency of RB-1 inactivation in ALL-patients ranged between 30% and 64% in several studies. Structural abnormalities of the RB-1 gene were reported in 18% of ALL-patients and in 27% of Philadelphia chromosome-positive ALL, respectively. The proportion of AML-patients with absent RB-1 protein expression ranged between 19% and 55%. Structural RB-1-abnormalities in AML were predominantly reported in leukemias with monocytic differentiation. Furthermore, the prognostic value of an abnormal RB-1 gene expression was also estimated in some studies. In childhood ALL RB-1 inactivation was reported to have prognostic significance while in contrast, in another study on adults no prognostic value of RB-1 was found. In 4 out of 5 documented studies AML-patients with RB-1 inactivation generally had a poorer prognosis. In conclusion, RB-1 inactivation is frequently observed in acute leukemia. The prognostic value of low RB-1 expression is controversial but the majority of published studies found low RB-1 expression to be a negative prognostic predictor, in acute leukemia.
Publication Types:
Review
PMID: 9517499 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
3: Leuk Lymphoma. 1995 Jun;18(1-2):61-7.
Abnormalities of retinoblastoma gene expression in hematological malignancies.
Zhu YM, Haynes AP, Keith FJ, Russell NH.
Department of Haematology, Nottingham City Hospital, U.K.
The human retinoblastoma gene product which is involved in cell cycle control and also acts as a transcriptional repressor of genes involved in growth control, is constitutively expressed as a phosphoprotein in normal hemopoietic cells. Abnormalities of the retinoblastoma gene expression leading to loss of protein expression either due to structural changes, mutations or transcriptional abnormalities have been found in a variety of hematological malignancies. There is evidence that loss of Rb protein expression is particularly associated with tumour progression and an adverse response to therapy which may be linked to the biological effect of Rb protein loss on the growth characteristics of tumour cells.
Publication Types:
Review
PMID: 8580830 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
4: Am J Pathol. 1992 Aug;141(2):363-75.
Expression of developmentally defined retinal phenotypes in the histogenesis of retinoblastoma.
Gonzalez-Fernandez F, Lopes MB, Garcia-Fernandez JM, Foster RG, De Grip WJ, Rosemberg S, Newman SA, VandenBerg SR.
Department of Pathology (Neuropathology), University of Virginia Health Sciences Center, Charlottesville 22908.
Retinoblastoma, the most common intraocular tumor of childhood, is a malignant neoplasm that arises during retinal development. The embryonal cell target for neoplastic transformation is not yet clearly defined. To better understand the histogenetic potential of this tumor, the expression of photoreceptor and glial cell-associated proteins were examined in 22 primary retinoblastomas. Interphotoreceptor retinol-binding protein (IRBP), cone and rod opsins were selected as the photoreceptor specific proteins due to their different temporal patterns of expression during normal retinal development. Neoplastic Müller cell differentiation, and non-neoplastic reactive astrocytes were identified using cellular retinaldehyde binding-protein (CRAlBP), and glial fibrillary acidic protein (GFAP), respectively. Photoreceptor proteins were present in 16 cases and showed different cellular patterns of expression. IRBP and cone opsin were usually abundant. Although rod opsin was clearly identified in eight tumors, its expression was more restricted than either IRBP or cone opsin. This differential pattern of expression, opposite to the normal pattern of photoreceptor gene expression in the adult retina, corresponded to a marked decrease in mRNA for rod opsin. Cone opsin and IRBP colocalized in fleurettes demonstrating that neoplastic human cone cells are capable of IRBP synthesis. Müller cell differentiation was present in 12 of the 16 cases in which photoreceptor proteins were detected. In contrast, GFAP was only present in reactive, stromal astrocytes associated with blood vessels. Our data suggest that the retinoblastoma has the histogenetic potential of the immature neural retinal epithelium which can give rise to both photoreceptor and Müller cell lineages. The differential expression of cone and rod phenotypes in retinoblastoma is consistent with the "default" mechanism of cone cell differentiation.
Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review
PMID: 1386715 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
5: Ophthalmic Paediatr Genet. 1987 Mar;8(1):3-10.
Retinoblastoma, chromosome abnormalities and oncogene expression.
Gilbert F, Potluri VR, Short MP, Kau CL, Lalatta F.
Recurrent chromosomal abnormalities in retinoblastomas involve numbers 13, 1, and 6, as well as homogeneously staining regions (HSR) and double minutes (DMS). Evidence suggesting that chromosome 13 contains a gene responsible for tumorigenesis has already been presented. We postulate that the genetic changes resulting from abnormalities of chromosomes 1 and 6 and the HSR/DMS provide a selective growth advantage to cells in which they occur. Support for this hypothesis, as it relates to the HSR/DMS and oncogene amplification, is discussed.
Publication Types:
Review
PMID: 3295640 [PubMed - indexed for MEDLINE]
| Navigate through the articles | |
Retinoblastoma Tumor Suppressor Protein Interactions
|
|
|
|