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

Genes Chromosomes and Cancer - Tập 45 Số 11 - Trang 1058-1069 - 2006
Xin Huang1,2, Tony E. Godfrey1,3,2, William E. Gooding2, Kenneth S. McCarty4,5,2, Susanne M. Gollin1,2
1Department of Human Genetics, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA 15261
2University of Pittsburgh Cancer Institute, Pittsburgh, PA 15232
3Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261
4Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261
5Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261

Tóm tắt

Abstract11q13 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. © 2006 Wiley‐Liss, Inc.

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Genes Chromosomes and Cancer

Tập 45 Số 11

1058-1069

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