© 2002 by Society
© 2002 by the Society forNeuro-Oncology
A chromosomal region 7p11.2 transcript map: Its development andapplication to the study of EGFR amplicons in glioblastoma
Department of Laboratory Medicine and Pathology (A.P.,R.B.J., C.D.J.) and Tumor Biology Program (G.D.E.,J.L.R., S.P., R.B.J., N.J.M., C.D.J.), Mayo Clinic, Rochester, MN55905
2 Address correspondence and reprint requests to C. David James, Department ofLaboratory Medicine and Pathology, Mayo Clinic, 200 First St., SW, HiltonBldg., Rm. 820 D, Rochester, MN 55905.
| Abstract |
|---|
Cumulative information available about the organization of amplifiedchromosomal regions in human tumors suggests that the amplification repeatunits, or amplicons, can be of a simple or complex nature. For the former,amplified regions generally retain their native chromosomal configuration andinvolve a single amplification target sequence. For complex amplicons,amplified DNAs usually undergo substantial reorganization relative to thenormal chromosomal regions from which they evolve, and the regions subject toamplification may contain multiple target sequences. Previous efforts tocharacterize the 7p11.2 epidermal growth factor receptor (EGFR)amplicon in glioblastoma have relied primarily on the use of markerspositioned by linkage analysis and/or radiation hybrid mapping, both of whichare known to have the potential for being inaccurate when attempting to orderloci over relatively short (<1 Mb) chromosomal regions. Due to the limitedresolution of genetic maps that have been established through the use of theseapproaches, we have constructed a 2-Mb bacterial and P1-derived artificialchromosome (BAC-PAC) contig for the EGFR region and have appliedmarkers positioned on its associated physical map to the analysis of 7p11.2amplifications in a series of glioblastomas. Our data indicate thatEGFR is the sole amplification target within the mapped region,although there are several additional 7p11.2 genes that can be coamplified andoverexpressed with EGFR. Furthermore, these results are consistentwith EGFR amplicons retaining the same organization as the nativechromosome 7p11.2 region from which they are derived.
Received October 11, 2001; Accepted January 2, 2002
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
Z. Lu, L. Zhou, P. Killela, A. B. Rasheed, C. Di, W. E. Poe, R. E. McLendon, D. D. Bigner, C. Nicchitta, and H. Yan Glioblastoma Proto-oncogene SEC61{gamma} Is Required for Tumor Cell Survival and Response to Endoplasmic Reticulum Stress Cancer Res., December 1, 2009; 69(23): 9105 - 9111. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. J.-C. Sheu, C.-H. Hua, L. Wan, Y.-J. Lin, M.-T. Lai, H.-C. Tseng, N. Jinawath, M.-H. Tsai, N.-W. Chang, C.-F. Lin, et al. Functional Genomic Analysis Identified Epidermal Growth Factor Receptor Activation as the Most Common Genetic Event in Oral Squamous Cell Carcinoma Cancer Res., March 15, 2009; 69(6): 2568 - 2576. [Abstract] [Full Text] [PDF] |
||||
![]() |
U. Fischer, A. Keller, P. Leidinger, S. Deutscher, S. Heisel, S. Urbschat, H.-P. Lenhof, and E. Meese A Different View on DNA Amplifications Indicates Frequent, Highly Complex, and Stable Amplicons on 12q13-21 in Glioma Mol. Cancer Res., April 1, 2008; 6(4): 576 - 584. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. H. Chung, K. Ely, L. McGavran, M. Varella-Garcia, J. Parker, N. Parker, C. Jarrett, J. Carter, B. A. Murphy, J. Netterville, et al. Increased Epidermal Growth Factor Receptor Gene Copy Number Is Associated With Poor Prognosis in Head and Neck Squamous Cell Carcinomas J. Clin. Oncol., September 1, 2006; 24(25): 4170 - 4176. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y.-H. Zhou, F. Tan, K. R. Hess, and W. K. A. Yung The Expression of PAX6, PTEN, Vascular Endothelial Growth Factor, and Epidermal Growth Factor Receptor in Gliomas: Relationship to Tumor Grade and Survival Clin. Cancer Res., August 1, 2003; 9(9): 3369 - 3375. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Park and C. D. James Lanthionine Synthetase Components C-like 2 Increases Cellular Sensitivity to Adriamycin by Decreasing the Expression of P-Glycoprotein through a Transcription-mediated Mechanism Cancer Res., February 1, 2003; 63(3): 723 - 727. [Abstract] [Full Text] [PDF] |
||||



