A region within murine chromosome 7F4, syntenic to the human 11q13 amplicon, is frequently amplified in 4NQO-induced oral cavity tumors&gt;

Yuan, Bo; Oechsli, Margaret; Hendler, F. J.

doi:10.1038/sj.onc.1201269

Cited by 22 publications

(19 citation statements)

References 37 publications

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“…By comparing the human and mouse DNA sequences, we found that the human 11q13 amplicon sequence matched a distinctive syntenic block in mouse chromosomal band 7F5. Interestingly, 7F5 is frequently amplified in 4-NQO-induced murine OSCC (Yuan et al, 1997). The well-matched synteny between the human 11q13 amplicon core and the mouse 7F5 amplicon suggests that during evolution, the genomic structure of the \cassette" of genes at 11q13 was conserved.…”

Section: Discussionmentioning

confidence: 95%

“…Genes at the distal end of mouse chromosomal region 7F5, Ccnd1, Fgf4, and Fgf3, are amplified frequently in 4-nitroquinoline-1-oxide (4NQO)-induced murine OSCC (Yuan et al, 1997). Therefore, we investigated whether synteny is present between the human OSCC 11q13 amplicon and mouse chromosomal band 7F5.…”

Section: The 11q13 Amplicon Is Syntenic To Mouse Chromosomal Band 7f5mentioning

confidence: 98%

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Comprehensive genome and transcriptome analysis of the 11q13 amplicon in human oral cancer and synteny to the 7F5 amplicon in murine oral carcinoma

Huang

Godfrey

Gooding

et al. 2006

Genes Chromosomes & Cancer

121

111

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11q13 amplification occurs in a wide variety of tumors, including almost half of oral squamous cell carcinomas (OSCC) where it has been correlated with a poor outcome. In this study, we compiled 3.6 Mb of DNA sequence in the 11q13 amplicon core and refined the physical map of the amplicon. In the process, we determined the genomic structure and normal tissue expression patterns of two recently identified genes, TAOS2/TMEM16A and MRGF, which reside in the amplicon core. We then quantified DNA copy number and mRNA expression of all genes in the 11q13 amplicon in cell lines and primary tumors from OSCC. With the exception of FGF3, FGF4, FGF19, and MRGF, all genes were overexpressed in most tumors with genomic amplification. Furthermore, we found that the expression of genes in the amplicon appeared to be highly coordinated, making it difficult to determine which gene or genes are driving amplification. However, in nonamplified primary tumors, three genes, TAOS2/TMEM16A, OCIM, and TPCN2, are frequently overexpressed, whereas CCND1 and EMS1 are not. These results suggest that in addition to CCND1 and EMS1, other important genes also may be target genes driving 11q13 amplification. We hypothesize that 11q13 amplification may be driven by a cassette of genes that provide growth or metastatic advantage to cancer cells. This is supported by the finding that the human 11q13 amplicon core is syntenic to mouse chromosomal band 7F5, which is frequently amplified in chemically induced murine OSCC. This article contains Supplementary Material available at http://www.interscience.wiley.com/jpages/1045-2257/suppmat

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Section: Discussionmentioning

confidence: 95%

Section: The 11q13 Amplicon Is Syntenic To Mouse Chromosomal Band 7f5mentioning

confidence: 98%

Comprehensive genome and transcriptome analysis of the 11q13 amplicon in human oral cancer and synteny to the 7F5 amplicon in murine oral carcinoma

Huang

Godfrey

Gooding

et al. 2006

Genes Chromosomes & Cancer

121

111

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“…Fusion of chromosomes during evolution might preferably occur at fragile regions and can be considered as possible breakpoint regions in the process of DNA ampliWcation (Yuan et al 1997). Therefore, we compared human chromosome 11 (hChr11) to homologous sequences of a number of sequenced mammals that are phylogenetically close to human (Fig.…”

Section: Amplicon Boundaries Are Xanked By Synteny Transitionsmentioning

confidence: 99%

High-resolution mapping identifies a commonly amplified 11q13.3 region containing multiple genes flanked by segmental duplications

et al. 2006

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DNA amplification of the 11q13 region is observed frequently in many carcinomas. Within the amplified region several candidate oncogenes have been mapped, including cyclin D1, TAOS1 and cortactin. Yet, it is unknown which gene(s) is/are responsible for the selective pressure enabling amplicon formation. This is probably due to the use of low-resolution detection methods. Furthermore, the size and structure of the amplified 11q13 region is complex and consists of multiple amplicon cores that differ between different tumor types. We set out to test whether the borders of the 11q13 amplicon are restricted to regions that enable DNA breakage and subsequent amplification. A high-resolution array of the 11q13 region was generated to study the structure of the 11q13 amplicon and analyzed 29 laryngeal and pharyngeal carcinomas and nine cell lines with 11q13 amplification. We found that boundaries of the commonly amplified region were restricted to four segments. Three boundaries coincided with a syntenic breakpoint. Such regions have been suggested to be putatively fragile. Sequence comparisons revealed that the amplicon was flanked by two large low copy repeats known as segmental duplications. These segmental duplications might be responsible for the typical structure and size of the 11q13 amplicon. We hypothesize that the selection for genes through amplification of the 11q13.3 region is determined by the ability to form DNA breaks within specific regions and, consequently, results in large amplicons containing multiple genes.

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“…Amplification of the Cyclin D1 locus, 11q13, has been reported in numerous epithelial malignancies. Approximately 30-50% of OSCC tumors show and amplification and/ or increased protein expression [60][61][62].…”

Section: Genetic Alteration In Preneoplastic Lesionsmentioning

confidence: 99%

Molecular mechanisms of head and neck cancer

Deshpande

Wong²

2008

Expert Review of Anticancer Therapy

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Background-With a global incidence rank of eight and a significant portion of head and neck malignancies (~90%), oral squamous cell carcinoma (OSCC) poses a major health risk and is one of the leading cause of mortality in developing nations [1]. Distribution of the incidence of OSCC varies across the world with south-central Asia and Africa leading, followed by eastern and central Europe, and to a lesser extent Australia, Japan, and the United States. Over the past few years there has been a drastic increase in the incidence of oral cancer in most parts of the world [2]. In the United States alone, with about 17 new cases/100,000, oral cancer is the fifth most common and sixth leading cause of cancer-related mortality per year [3].While men tend to have a higher incidence of OSCC (6.6/100,000) compared to women (2.9/100,000), there is an equal mortality rate between the sexes (50%).

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A region within murine chromosome 7F4, syntenic to the human 11q13 amplicon, is frequently amplified in 4NQO-induced oral cavity tumors>

Cited by 22 publications

References 37 publications

Comprehensive genome and transcriptome analysis of the 11q13 amplicon in human oral cancer and synteny to the 7F5 amplicon in murine oral carcinoma

Comprehensive genome and transcriptome analysis of the 11q13 amplicon in human oral cancer and synteny to the 7F5 amplicon in murine oral carcinoma

High-resolution mapping identifies a commonly amplified 11q13.3 region containing multiple genes flanked by segmental duplications

Molecular mechanisms of head and neck cancer

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