PT  - JOURNAL ARTICLE
AU  - Li, Aiguo
AU  - Walling, Jennifer
AU  - Kotliarov, Yuri
AU  - Center, Angela
AU  - Steed, Mary Ellen
AU  - Ahn, Susie J.
AU  - Rosenblum, Mark
AU  - Mikkelsen, Tom
AU  - Zenklusen, Jean Claude
AU  - Fine, Howard A.
TI  - Genomic Changes and Gene Expression Profiles Reveal That Established Glioma Cell Lines Are Poorly Representative of Primary Human Gliomas
AID  - 10.1158/1541-7786.MCR-07-0280
DP  - 2008 Jan 01
TA  - Molecular Cancer Research
PG  - 21--30
VI  - 6
IP  - 1
4099  - http://mcr.aacrjournals.org/content/6/1/21.short
4100  - http://mcr.aacrjournals.org/content/6/1/21.full
SO  - Mol Cancer Res2008 Jan 01; 6
AB  - Genetic aberrations, such as gene amplification, deletions, and loss of heterozygosity, are hallmarks of cancer and are thought to be major contributors to the neoplastic process. Established cancer cell lines have been the primary in vitro and in vivo models for cancer for more than 2 decades; however, few such cell lines have been extensively characterized at the genomic level. Here, we present a high-resolution genome-wide chromosomal alteration and gene expression analyses of five of the most commonly used glioma cell lines and compare the findings with those observed in 83 primary human gliomas. Although genomic alterations known to occur in primary tumors were identified in the cell lines, we also observed several novel recurrent aberrations in the glioma cell lines that are not frequently represented in primary tumors. Additionally, a global gene expression cluster distinct from primary tumors was identified in the glioma cell lines. Our results indicate that established cell lines are generally a poor representation of primary tumor biology, presenting a host of genomic and gene expression changes not observed in primary tissues, although some discrete features of glioma biology were conserved in the established cell lines. Refined maps of genetic alterations and transcriptional divergence from the original tumor type, such as the one presented here, may help serve as a guideline for a more biologically rational and clinically relevant selection of the most appropriate glioma model for a given experiment. (Mol Cancer Res 2008;6(1):21–30)