Loss of heterozygosity at 7q31.1 and 12p13‐12 in advanced prostate cancer

Kawana, Yoko; Ichikawa, Tomohiko; Suzuki, Hiroyoshi; Ueda, Takeshi; Komiya, Akira; Ichikawa, Yoshiyasu; Furuya, Yuzo; Akakura, Koichiro; Igarashi, Tatsuo; Itô, Haruo

doi:10.1002/pros.10131

Cited by 26 publications

(20 citation statements)

References 22 publications

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“…ENCODE region ENm001 corresponds to chromosome 7q31, which is known as a fragile site with frequent loss of heterozygosity in advanced prostate cancer (Kawana et al, 2002). Among several genes at 7q31, TES (testis-derived transcript) has been shown as a candidate tumor suppressor gene in prostate cancer (Chene et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Identification of novel androgen response genes in prostate cancer cells by coupling chromatin immunoprecipitation and genomic microarray analysis

et al. 2007

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The androgen receptor (AR) plays a key role as a transcriptional factor in prostate development and carcinogenesis. Identification of androgen-regulated genes is essential to elucidate the AR pathophysiology in prostate cancer. Here, we identified androgen target genes that are directly regulated by AR in LNCaP cells, by combining chromatin immunoprecipitation (ChIP) with tiling microarrays (ChIP-chip). ChIP-enriched or control DNAs from the cells treated with R1881 were hybridized with the ENCODE array, in which a set of regions representing approximately 1% of the whole genome. We chose 10 bona fide AR-binding sites (ARBSs) (Po1e-5) and validated their significant AR recruitment ligand dependently. Eight upregulated genes by R1881 were identified in the vicinity of the ARBSs. Among the upregulated genes, we focused on UGT1A and CDH2 as AR target genes, because the ARBSs close to these genes (in UGT1A distal promoter and CDH2 intron 1) were most significantly associated with acetylated histone H3/H4, RNA polymerase II and p160 family co-activators. Luciferase reporter constructs including those two ARBSs exhibited ligand-dependent transcriptional regulator/enhancer activities. The present study would be powerful to extend our knowledge of the diversity of androgen genetic network and steroid action in prostate cancer cells.

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Section: Discussionmentioning

confidence: 99%

Identification of novel androgen response genes in prostate cancer cells by coupling chromatin immunoprecipitation and genomic microarray analysis

et al. 2007

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“…Both amplification and deletion in the region has previously been suggested. [30][31][32][33] To further delineate the specific form of chromosomal alteration pinpointed to by SMAL-PCR DNA fingerprinting analysis at 12p12.1, leading to overexpression of SOX5, FISH analysis was carried out on whole-mount formalin-fixed paraffin-embedded sections from 12 patient cases showing either no, low or high SOX5 expression, as detected by IHC analyses. SOX5 amplification was not detected in the normal or BPH tissue specimens while amplification was evident in 1 of 2 prostate tumor cases showing low SOX5 expression; and 5 of 8 cases showing high SOX5 expression (Fig.…”

Section: Sox5 Overexpression Is a Results Of Gene Amplification At 12pmentioning

confidence: 99%

DNA fingerprinting tags novel altered chromosomal regions and identifies the involvement of SOX5 in the progression of prostate cancer

Chan

Woolcock

et al. 2009

Intl Journal of Cancer

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Identification of genomic alterations associated with the progression of prostate cancer may facilitate the better understanding of the development of this highly variable disease. Matched normal, premalignant high-grade prostatic intraepithelial neoplasia and invasive prostate carcinoma cells were procured by laser capture microdissection (LCM) from human radical prostatectomy specimens. From these cells, comparative DNA fingerprints were generated by a modified PCR-based technique called scanning of microdissected archival lesion (SMAL)-PCR. Recurrent polymorphic fingerprint fragments were used in tagging altered chromosomal regions. Altered regions were found at cytobands 1p31. 3, 1q44, 2p23.1, 3p26.3, 3q22.3, 4q22.3, 4q35.2, 5q23.2, 8q22.3, 8q24.13, 9q21.3, 9q22.32, 10q11.21, 11p13, 12p12.1, 13q12.1, 16q12.2 and 18q21.31. Candidate genes in the surrounding area that may possibly harbor mutations that change normal prostatic cells to progress into their tumor stages were proposed. Of these fragments, a 420 bp alteration, absent in all 26 normal samples screened, was observed in 2 tumors. This fragment was cloned, sequenced and localized to chromosome 12p12.1. Within this region, candidate gene sex determining region Y-box 5 (SOX5) was proposed. Further studies of SOX5 in cell lines, xenografts and human prostate specimens, at both the RNA and protein levels, found overexpression of the gene in tumors. This overexpression was then subsequently found by fluorescent in situ hybridization to be caused by amplification of the region. In conclusion, our results suggest LCM coupled with SMAL-PCR DNA fingerprinting is a useful method for the screening and identification of chromosomal regions and genes associated with cancer development. Further, overexpression of SOX5 is associated with prostate tumor progression and early development of distant metastasis.

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“…Loss of heterozygosity in 12p13 that includes the ING4 gene has been reported in 5-26% of childhood acute lymphoblastic leukemia (25)(26)(27), 12-43% of prostate cancer (28,29), and 26% of ovarian cancer (30). This chromosomal region also carries two other candidate tumor suppressors, TEL͞ETV6 and p27KIP, at 11.8 and 12.7 Mb from the telomere, respectively.…”

Section: Ing4 Maps To a Region Frequently Deleted In Humanmentioning

confidence: 99%

A screen for genes that suppress loss of contact inhibition: Identification of ING4 as a candidate tumor suppressor gene in human cancer

Kim

Chin

Gray

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

130

192

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Loss of heterozygosity at 7q31.1 and 12p13‐12 in advanced prostate cancer

Cited by 26 publications

References 22 publications

Identification of novel androgen response genes in prostate cancer cells by coupling chromatin immunoprecipitation and genomic microarray analysis

Identification of novel androgen response genes in prostate cancer cells by coupling chromatin immunoprecipitation and genomic microarray analysis

DNA fingerprinting tags novel altered chromosomal regions and identifies the involvement of SOX5 in the progression of prostate cancer

A screen for genes that suppress loss of contact inhibition: Identification of ING4 as a candidate tumor suppressor gene in human cancer

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