Mapping of metastasis suppressor gene(s) for rat prostate cancer on the short arm of human chromosome 8 by irradiated microcell-mediated chromosome transfer

Nihei, Naoki; Ichikawa, Tomohiko; Kawana, Youko; Kuramochi, Hiroaki; Kugoh, Hiroyuki; Oshimura, Mitsuo; Hayata, Isamu; Shimazaki, Jun; Itô, Haruo

doi:10.1002/(sici)1098-2264(199612)17:4<260::aid-gcc8>3.0.co;2-1

Cited by 39 publications

(20 citation statements)

References 19 publications

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“…The BNIP3L gene is located between markers D8S1752 and D8S1989 that map to 8p21 in the smallest region of overlap (SRO) identified by LOH analysis of breast and ovarian tumours (Seitz et al, 2000;Brown et al, 1999), and to a region of prostate cancer metastasis suppression (Nihei et al, 1996). BNIP3L encodes a protein that is homologous to the proapoptotic protein BNIP3 (Matsushima et al, 1998;Chen et al, 1999;Imazu et al, 1999;Yasuda et al, 1999).…”

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Analysis of the candidate 8p21 tumour suppressor, BNIP3L, in breast and ovarian cancer

et al. 2003

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Loss of heterozygosity (LOH) on the short arm of chromosome 8, at 8p12 -p23, is one of the most frequent genetic events in both breast and ovarian cancer, suggesting the location of a shared tumour suppressor gene. Microcell-mediated chromosome transfer of chromosome 8 suppresses tumorigenicity and growth of colorectal and prostate cancer cell lines, further supporting the presence of a tumour suppressor gene on 8p. We have taken a candidate gene approach to try to identify this tumour suppressor gene at 8p12 -p23. BNIP3L, which has sequence homology to pro-apoptotic proteins and the ability to suppress colony formation in soft agar, is located at 8p21, within a region of ovarian cancer LOH, breast cancer LOH and prostate cancer metastasis suppression. BNIP3L expression was assessed by both RT -PCR and Northern blot analysis in breast and ovarian cancer cell lines and found to be expressed at similar levels relative to expression in their respective normal epithelial cell lines. Genetic analysis of BNIP3L in 40 primary ovarian and 25 primary breast tumours identified one somatic, intronic mutation in one ovarian tumour, as well as several polymorphisms, including one resulting in an amino-acid substitution. These data suggest that BNIP3L is unlikely to be the target of 8p LOH in ovarian or breast cancer.

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Analysis of the candidate 8p21 tumour suppressor, BNIP3L, in breast and ovarian cancer

et al. 2003

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“…In prostate cancer, loss of heterozygosity (LOH) for markers on 8p is one of the most frequent somatic mutations, occurring in >60% of these tumors (Cunningham et al 1996). Functional evidence that chromosome 8 contains tumor suppressor gene-associated activity is provided by microcell-mediated chromosome transfer studies, which demonstrate suppression by this chromosome of in vivo metastatic ability and in vitro invasiveness in the highly metastatic rat prostate cancer cell line AT6.2 (Nihei et al 1996;Kuramochi et al 1997), suppression of both tumorigenicity and in vitro invasiveness in the COKFu colon carcinoma cell line (Tanaka et al 1996), reduction of tumorigenicity in the SW620 colon carcinoma cell line, and total suppression of soft agar clonicity in the HT29 colon carcinoma cell line (Gustafson et al 1996). Together, these studies strongly suggest that 8p harbors a tumor suppressor gene involved in the genesis of epithelial malignancies.…”

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High-Resolution Physical Map and Transcript Identification of a Prostate Cancer Deletion Interval on 8p22

Arbieva¹,

Banerjee²,

Kim³

et al. 2000

Genome Res.

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A genomic interval of ∼1-1.5 Mb centered at the MSR marker on 8p22 has emerged as a possible site for a tumor suppressor gene, based on high rates of allele loss and the presence of a homozygous deletion found in metastatic prostate cancer. The objective of this study was to prepare a bacterial contig of this interval, integrate the contig with radiation hybrid (RH) databases, and use these resources to identify transcription units that might represent the candidate tumor suppressor genes. Here we present a complete bacterial contig across the interval, which was assembled using 22 published and 17 newly originated STSs. The physical map provides twofold or greater coverage over much of the interval, including 17 BACs, 15 P1s, 2 cosmids, and 1 PAC clone. The position of the selected markers across the interval in relation to the other markers on the larger chromosomal scale was confirmed by RH mapping using the Stanford G3 RH panel. Transcribed units within the deletion region were identified by exon amplification, searching of the Human Transcript Map, placement of unmapped expressed sequence tags (ESTs) from the Radiation Hybrid Database (RHdb), and from other published sources, resulting in the isolation of six unique expressed sequences. The transcript map of the deletion interval now includes two known genes (MSR and N33) and six novel ESTs.

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“…Hotspots of genomic deletion may therefore indicate the areas where tumor suppressor genes are more likely to reside. Chromosome 8p deletions are frequently observed in many human cancers including prostate, colorectal, bladder, head and neck, breast, and gastric carcinomas (3)(4)(5)(6)(7)(8) and the 8p22 region has been shown to possess oncosuppressive properties in chromosome transfer experiments (9)(10)(11). Genes isolated from this area include N33 (12,13), PRLTS (14,15), NAT1, NAT2 (16)(17)(18) etc., but there is little functional evidence for their involvement in human cancer.…”

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confidence: 99%

Reduced FEZ1/LZTS1 Expression and Outcome Prediction in Lung Cancer

et al. 2005

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Chromosomal deletions are often observed in lung cancers suggesting that inactivation of tumor suppressor genes plays an important role in the development of this neoplasm. The region around chromosome 8p22 is a frequent and early target of these deletions and has therefore been investigated for the presence of candidate genes. The FEZ1/LZTS1 gene, located at 8p22, is inactivated in many cancers with 8p deletions, including prostate, esophageal, gastric, bladder, and breast cancer and the Fez1 protein has been shown to suppress growth of cancer cells and to regulate mitosis. To elucidate the role of FEZ1 in lung cancer, we have analyzed its expression by immunohistochemistry in 103 primary lung cancer specimens including 98 non-small cell lung cancers (57 adenocarcinomas, 32 squamous cell carcinomas, 7 large cell carcinomas, and 2 others) and five small cell carcinomas. Absence of Fez1 protein expression was observed in 27 cases (26%) and additional 43 cases (42%) showed strong reduction in immunoreactivity. There was a positive association between loss of FEZ1 expression and tumor grading (P = 0.0345) and a tendency toward a reduction in the mortality rate in subjects with strong FEZ1 expression. Overall, these data indicate an important role for FEZ1 in lung cancer and suggest the possibility that it may serve as a novel prognostic indicator. (Cancer Res 2005; 65(4): 1207-12)

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Mapping of metastasis suppressor gene(s) for rat prostate cancer on the short arm of human chromosome 8 by irradiated microcell-mediated chromosome transfer

Cited by 39 publications

References 19 publications

Analysis of the candidate 8p21 tumour suppressor, BNIP3L, in breast and ovarian cancer

Analysis of the candidate 8p21 tumour suppressor, BNIP3L, in breast and ovarian cancer

High-Resolution Physical Map and Transcript Identification of a Prostate Cancer Deletion Interval on 8p22

Reduced FEZ1/LZTS1 Expression and Outcome Prediction in Lung Cancer

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