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Alterations of BCCIP, a BRCA2 interacting protein, in astrocytomas

BACKGROUND: Loss of heterozygosity of chromosome 10q26 has been shown to be associated with the aggressiveness of astrocytic tumors (or astrocytomas), but the responsible gene(s) residing in this region has not been fully identified. The BCCIP gene is located at chromosome 10q26. It encodes a BRCA2...

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Autores principales: Liu, Jingmei, Lu, Huimei, Ohgaki, Hiroko, Merlo, Adrian, Shen, Zhiyuan
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2736977/
https://www.ncbi.nlm.nih.gov/pubmed/19653894
http://dx.doi.org/10.1186/1471-2407-9-268
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author Liu, Jingmei
Lu, Huimei
Ohgaki, Hiroko
Merlo, Adrian
Shen, Zhiyuan
author_facet Liu, Jingmei
Lu, Huimei
Ohgaki, Hiroko
Merlo, Adrian
Shen, Zhiyuan
author_sort Liu, Jingmei
collection PubMed
description BACKGROUND: Loss of heterozygosity of chromosome 10q26 has been shown to be associated with the aggressiveness of astrocytic tumors (or astrocytomas), but the responsible gene(s) residing in this region has not been fully identified. The BCCIP gene is located at chromosome 10q26. It encodes a BRCA2 and CDKN1A (p21) interacting protein. Previous studies have shown that down-regulation of BCCIP impairs recombinational DNA repair, G1/S cell cycle checkpoint, p53 trans-activation activity, cytokinesis, and chromosome stability, suggesting a potential role of BCCIP in cancer etiology. In this study, we investigated whether BCCIP is altered in astrocytomas. METHODS: Genomic DNA from 45 cases of grade IV astrocytic tumor (glioblastoma) tissues and 12 cases of normal tissues were analyzed by quantitative PCR. The BCCIP protein expression in 96 cases of grade II–IV astrocytic tumors was detected by immunohistochemistry (IHC). IHC staining of glial fibrillary acid protein (GFAP), a marker for astrocytic cells, was used to identify cells of the astrocytic lineage. RESULTS: We found that BCCIP protein is expressed in normal cells with positive staining of GFAP. However, BCCIP protein expression was not detectable in ~45% of all astrocytic tumors, and in > 60% in the grade IV glioblastoma. About 45% glioblastoma have significant (p < 0.01) reduction of BCCIP gene copy number when compared to normal DNA. Furthermore, the frequency of lacking BCCIP expression is associated with the aggressiveness of astrocytic tumors. CONCLUSION: Our data implicate a role of BCCIP in astrocytic tumorigenesis, and lack of BCCIP may be used as a marker for astrocytomas.
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spelling pubmed-27369772009-09-03 Alterations of BCCIP, a BRCA2 interacting protein, in astrocytomas Liu, Jingmei Lu, Huimei Ohgaki, Hiroko Merlo, Adrian Shen, Zhiyuan BMC Cancer Research Article BACKGROUND: Loss of heterozygosity of chromosome 10q26 has been shown to be associated with the aggressiveness of astrocytic tumors (or astrocytomas), but the responsible gene(s) residing in this region has not been fully identified. The BCCIP gene is located at chromosome 10q26. It encodes a BRCA2 and CDKN1A (p21) interacting protein. Previous studies have shown that down-regulation of BCCIP impairs recombinational DNA repair, G1/S cell cycle checkpoint, p53 trans-activation activity, cytokinesis, and chromosome stability, suggesting a potential role of BCCIP in cancer etiology. In this study, we investigated whether BCCIP is altered in astrocytomas. METHODS: Genomic DNA from 45 cases of grade IV astrocytic tumor (glioblastoma) tissues and 12 cases of normal tissues were analyzed by quantitative PCR. The BCCIP protein expression in 96 cases of grade II–IV astrocytic tumors was detected by immunohistochemistry (IHC). IHC staining of glial fibrillary acid protein (GFAP), a marker for astrocytic cells, was used to identify cells of the astrocytic lineage. RESULTS: We found that BCCIP protein is expressed in normal cells with positive staining of GFAP. However, BCCIP protein expression was not detectable in ~45% of all astrocytic tumors, and in > 60% in the grade IV glioblastoma. About 45% glioblastoma have significant (p < 0.01) reduction of BCCIP gene copy number when compared to normal DNA. Furthermore, the frequency of lacking BCCIP expression is associated with the aggressiveness of astrocytic tumors. CONCLUSION: Our data implicate a role of BCCIP in astrocytic tumorigenesis, and lack of BCCIP may be used as a marker for astrocytomas. BioMed Central 2009-08-04 /pmc/articles/PMC2736977/ /pubmed/19653894 http://dx.doi.org/10.1186/1471-2407-9-268 Text en Copyright ©2009 Liu et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Liu, Jingmei
Lu, Huimei
Ohgaki, Hiroko
Merlo, Adrian
Shen, Zhiyuan
Alterations of BCCIP, a BRCA2 interacting protein, in astrocytomas
title Alterations of BCCIP, a BRCA2 interacting protein, in astrocytomas
title_full Alterations of BCCIP, a BRCA2 interacting protein, in astrocytomas
title_fullStr Alterations of BCCIP, a BRCA2 interacting protein, in astrocytomas
title_full_unstemmed Alterations of BCCIP, a BRCA2 interacting protein, in astrocytomas
title_short Alterations of BCCIP, a BRCA2 interacting protein, in astrocytomas
title_sort alterations of bccip, a brca2 interacting protein, in astrocytomas
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2736977/
https://www.ncbi.nlm.nih.gov/pubmed/19653894
http://dx.doi.org/10.1186/1471-2407-9-268
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