Positional cloning of
 ZNF
 217
 and
 NABC
 1
 : Genes amplified at 20q13.2 and overexpressed in breast carcinoma

Collins, Colin C.; Rommens, Johanna M.; Kowbel, David; Godfrey, Tony E.; Tanner, Minna; Hwang, Soo In; Polikoff, Daniel; Nonet, Genevieve H.; Cochran, Joanne; Myambo, Ken; Jay, Karen E.; Froula, Jeff; Cloutier, Thomas; Kuo, Wen Lin; Yaswen, Paul; Dairkee, Shanaz H.; Giovanola, Jennifer; Hutchinson, Gordon B.; Isola, Jorma; Kallioniemi, Olli; Palazzolo, M.; Martin, Chris; Ericsson, Cheryl L.; Pinkel, Dan; Albertson, Donna G.; Li, Wu Bo; Gray, Joe W.

doi:10.1073/pnas.95.15.8703

Cited by 266 publications

(219 citation statements)

References 38 publications

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“…In our study, the TRAF4 gain observed in 22% of all cases was moderate (up to 10 copies) but it was significantly associated with gene expression. The common criterion for designating a gene as a putative Amplification and overexpression of TRAF4 in cancer S Camilleri-Broët et al target of an amplicon is that amplification leads to its overexpression (Collins et al, 1998). We show that amplification represents one of the mechanisms leading to overexpression of the TRAF4 protein in most cancer types tested.…”

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confidence: 79%

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TRAF4 overexpression is a common characteristic of human carcinomas

et al. 2006

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Tumor necrosis factor receptor (TNFR) associated factor 4 (TRAF4) was initially identified as a gene amplified and overexpressed in breast carcinomas. Our aim was to evaluate whether TRAF4 protein overexpression exists in other cancer types. Immunohistochemistry analysis of tumor samples from 623 patients with 20 different tumor types showed that TRAF4 was overexpressed in 268 tumors (43%), including 82 of 137 lung adenocarcinomas (60%). Interestingly, 32 primary tumors and their matching metastases exhibited mostly similar TRAF4 expression pattern. TRAF4 protein overexpression was limited to cancer cells and the subcellular localization was consistently cytoplasmic in a large majority of cases. To investigate changes in TRAF4 gene copy number, 125 cases from six different types of carcinomas were also analysed by fluorescence in situ hybridization. Out of the 28 cases (22%) showing an increased TRAF4 gene copy number, 23 (82%) were overexpressing the protein. Thus, TRAF4 gene amplification is one of the mechanisms responsible for TRAF4 protein overexpression in human cancers. Considering that TRAF4 is located at 17q11.2 in a region of amplification devoid of known oncogenes and is commonly overexpressed in cancer, our data support an oncogenic role for TRAF4. Oncogene Keywords: TRAF4; chromosome 17q11; ERBB2; amplification; lung TRAF proteins belong to a family of cytoplasmic adaptors involved in the signalling cascade activated by receptors of the TNFR and interleukin-1/Toll-like receptor (IL-1R/TLR) families (Chung et al., 2002). Six TRAF proteins that share common structural features, including a carboxy-terminal TRAF domain, are encoded by the mammalian genome. Their main functions are exerted in the immune system where they regulate intracellular signalling pathways leading to the activation of a common set of transcription factors including NF-kB and AP-1 (Aggarwal, 2003).Unlike other members of the TRAF family, the biological function of TRAF4 remains elusive. Several reports suggested that TRAF4 could be recruited to different TNFR and TLR signalling pathways (Krajewska et al., 1998;Ye et al., 1999;Esparza and Arch, 2004;Takeshita et al., 2005), and in mitogen-activated protein kinase (MAPK) pathways (Xu et al., 2002;Abell and Johnson, 2005;Li et al., 2005) but in vivo evidence of such a role is still missing. Mice deficient for TRAF4 exhibit clear ontogenic defects affecting neural tube closure, tracheal formation and skeletal patterning, phenotypes that might be linked to abnormal cell migration (Regnier et al., 2002).TRAF4 was the first member of the TRAF protein family found upregulated in human carcinomas. Indeed, the TRAF4 cDNA was initially isolated from metastatic breast cancer Tomasetto et al., 1995), where the TRAF4 gene was amplified, leading to overexpression of the gene product (Bieche et al., 1996). Detailed analysis of the amplification pattern of five genes located on the long arm of the chromosome 17, including the ERBB2 oncogene (Slamon et al., 1989), revealed the existence of at least...

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confidence: 79%

“…Oncogene target of an amplicon is that amplification leads to its overexpression (Collins et al, 1998). We show that amplification represents one of the mechanisms leading to overexpression of the TRAF4 protein in most cancer types tested.…”

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confidence: 83%

TRAF4 overexpression is a common characteristic of human carcinomas

et al. 2006

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“…This issue is supported by recent molecular studies of the 20q region, the only amplification site discovered by CGH that has so far been extensively studied. Many potential target genes, including serine-threonine kinase BTAK/Aurora II (Sen et al, 1997;Bischoff et al, 1998), steroid receptor co-activator AIB1 (Anzick et al, 1997), MYBL2 oncogene (Kononen et al, 1998) PTPN1 phosphotyrosine phosphorylase (Tanner et al, 1996), as well as ZNF217 and NABC1 (Collins et al, 1998) genes have been found to be involved in DNA amplifications at 20q. …”

Section: Discussionmentioning

confidence: 99%

Molecular cytogenetic analysis of 11 new breast cancer cell lines

et al. 1999

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We describe a survey of genetic changes by comparative genomic hybridization (CGH) in 11 human breast cancer cell lines recently established in our laboratory. The most common gains took place at 8q (73%), 1q (64%), 7q (64%), 3q (45%) and 7p (45%), whereas losses were most frequent at Xp (54%), 8p (45%), 18q (45%) and Xq (45%). Many of the cell lines displayed prominent, localized DNA amplifications by CGH. One-third of these loci affected breast cancer oncogenes, whose amplifications were validated with specific probes: 17q12 (two cell lines with ERBB2 amplifications), 11q13 (two with cyclin-D1), 8p11–p12 (two with FGFR1) and 10q25 (one with FGFR2). Gains and amplifications affecting 8q were the most common genetic alterations in these cell lines with the minimal, common region of involvement at 8q22–q23. No high-level MYC (at 8q24) amplifications were found in any of the cell lines. Two-thirds of the amplification sites took place at loci not associated with established oncogenes, such as 1q41–q43, 7q21–q22, 7q31, 8q23, 9p21–p23, 11p12–p14, 15q12–q14, 16q13–q21, 17q23, 20p11–p12 and 20q13. Several of these locations have not been previously reported and may harbour important genes whose amplification is selected for during cancer development. In summary, this set of breast cancer cell lines displaying prominent DNA amplifications should facilitate discovery and functional analysis of genes and signal transduction pathways contributing to breast cancer development. © 1999 Cancer Research Campaign

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“…In addition, a novel zinc finger gene mapped on 20q13.2 was amplified in human breast cancer. 43 This leads to 2 hypotheses: (i) gain at 20q is a prognostic marker for primary colorectal cancer or (ii) several candidate genes (AIB1, BTAK/Aurora2, DcR3, etc.) identified within this location are associated with metastases of gastrointestinal cancer.…”

Section: Discussionmentioning

confidence: 99%

Chromosomal aberrations in colorectal cancers and liver metastases analyzed by comparative genomic hybridization

et al. 2001

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Comparative genomic hybridization (CGH) was used to screen for changes in the number of DNA sequence copies in 30 primary colorectal cancers and 16 liver metastases, to identify regions that contain genes important for the development and progression of colorectal cancer. In primary colorectal cancer, we found frequent gains at 7p21 (36.7%), 7q31-36 (30%), 8q23-24 (43.0%), 12p (30%) Many detailed reports have been published on the carcinogenesis of colorectal cancer. Several genetic aberrations are required for tumor initiation and progression. 1 These aberrations include activation of the SRC and RAS oncogenes 2,3 along with inactivation of the FAP 4,5 and DCC 6 tumor suppressors and loss of TP53 function. 7 However, genetic changes involved in the progression and metastases of colorectal cancer remain unclear. To investigate differences in chromosomal aberrations between primary colorectal cancer and metastatic liver tumor, we used comparative genomic hybridization (CGH). CGH is based on dual-color fluorescence in situ hybridization (FISH) using differentially labeled tumors and reference DNA as a probe. 8,9 The efficacy of CGH is based on the concept that regions with an increase in the number of copies reveal sites that may contain dominantly acting oncogenes, whereas regions with a reduction may harbor putative tumorsuppressor genes. 8 Our aim was to generate a comprehensive picture of genomic and chromosomal aberrations that occur during the development of metastases of colorectal cancers and to identify those chromosomal regions that contain genes important for the development and progression of colorectal cancer.,Colorectal adenoma and adenocarcinoma have previously been analyzed by CGH, 10 as have primary and metastatic liver tumors. 11,12 These results supported ours; above all, we emphasize that some important genes appear to be contained in 20q and to play an important role in liver metastases. Furthermore, we examined the follow-up surveys of all cases and compared cases with and without loss at 18q and with gains at 8q and 20q to determine the usefulness of these genetic alterations as prognostic markers. MATERIAL AND METHODS Samples and DNA preparationPrimary tumors and metastatic liver tumors from 44 cancer patients with colorectal cancer (Table I) were classified according to the UICC system. These samples were provided by the Department of Digestive Surgery, Kyoto Prefectural University of Medicine (Kyoto, Japan). After surgical resection, tissues were frozen and stored at -80°C and DNA was extracted. CGHCGH was performed as described previously. 13 In brief, tumor DNA was labeled with FITC-dUTP and controlled DNA and extracted from a normal male with the aid of Texas red-dUTP using nick translation. Metaphase spreads were denatured at 75°C for 2.1 min in a formamide solution [70% formamide, 2 ϫ SCC (pH 7.0)] and dehydrated in an ethanol series of 70%, 85% and 100%. Labeled tumor and normal DNAs together with 10 g unlabeled cot-1 DNA was mixed with 50% formamide, 10% dextran sulfate and 2 ϫ SSC...

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Positional cloning of ZNF 217 and NABC 1 : Genes amplified at 20q13.2 and overexpressed in breast carcinoma

Cited by 266 publications

References 38 publications

TRAF4 overexpression is a common characteristic of human carcinomas

TRAF4 overexpression is a common characteristic of human carcinomas

Molecular cytogenetic analysis of 11 new breast cancer cell lines

Chromosomal aberrations in colorectal cancers and liver metastases analyzed by comparative genomic hybridization

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