Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2008 Apr;44(4):369-82.
doi: 10.1016/j.oraloncology.2007.05.003. Epub 2007 Aug 2.

Chromosomal imbalances in oral squamous cell carcinoma: examination of 31 cell lines and review of the literature

Christa Lese Martin  1 , Shalini C Reshmi, Thomas Ried, William Gottberg, John W Wilson, Jaya K Reddy, Poornima Khanna, Jonas T Johnson, Eugene N Myers, Susanne M Gollin
Affiliations
Review

Chromosomal imbalances in oral squamous cell carcinoma: examination of 31 cell lines and review of the literature

Christa Lese Martin et al. Oral Oncol. 2008 Apr.

Abstract

Classical and molecular cytogenetic analysis, including fluorescence in situ hybridization (FISH) and chromosomal comparative genomic hybridization (CGH), were used to examine genetic changes involved in the development and/or progression of oral squamous cell carcinoma (OSCC). Of 31 OSCC cell lines studied, more than one-third expressed clonal structural abnormalities involving chromosomes 3, 7, 8, 9, and 11. Eleven OSCC cell lines were evaluated using CGH to identify novel genome-wide gains, losses, or amplifications. By CGH, more than half of the cell lines showed loss of 3p, gain of 3q, 8q, and 20q. Further, molecular cytogenetic analyses by FISH of primary tumors showed that the karyotypes of cell lines derived from those tumors correlated with specific gains and losses in the tumors from which they were derived. The most frequent nonrandom aberration identified by both karyotype and CGH analyses was amplification of chromosomal band 11q13 in the form of a homogeneously staining region. Our data suggest that loss of 9p and 11q13 amplification may be of prognostic benefit in the management of OSCC, which is consistent with the literature. The results of this study validate the relationship between these OSCC cell lines and the tumors from which they were derived. The results also emphasize the usefulness of these cell lines as in vitro experimental models and provide important genetic information on these OSCC cell lines that were recently reported in this journal.

PubMed Disclaimer

Conflict of interest statement

Conflict of interest

None of the authors have any financial or personal relationships with other people or organizations that could inappropriately influence or bias their contribution to this paper.

Figures

Figure 1
Figure 1
Representative karyotype from UPCI:SCC103 passage 10: 63<3n>,-X,-X, -Y,+der(2)t(2;?)(q10;?), −3, −4−5,i(5)(p10),+del(7)(q22), −8, −8,i(8)(q10),+10, +del(10)(q23),+der(11)(pter→q13::hsr::q14→q25::hsr::?), −13,+der(14)t(11;14)(q11;p11), −15, −16,der(16)t(16;17)(q24;q21), −17,del(17)(p11.1), −18,+20, −21, −21, −22, −22,+mar1, +mar2,+mar,+dmin.
Figure 2
Figure 2
Summary of nonrandom chromosomal losses and gains identified by classical cytogenetic analysis of thirty OSCC cell lines. The cell line number corresponding to each line is marked above the lines. Lines to the left or right of the ideograms indicate regions of loss and gain, respectively. Thick lines denote gene amplification.
Figure 3
Figure 3
Summary of nonrandom chromosomal losses and gains identified by chromosomal CGH in 11 OSCC cell lines. The cell line number corresponding to each line is marked above the lines. Lines to the left or right of the ideograms indicate regions of loss and gain, respectively. Thick lines denote gene amplification.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Jemal A, Siegel R, Ward E, Murray T, Xu J, et al. Cancer Statistics, 2007. CA Cancer J Clin. 2007;57(1):43–66. - PubMed
    1. Jemal A, Tiwari RC, Murray T, Ghafoor A, Samuels A, et al. Cancer Statistics, 2004. CA Cancer J Clin. 2004;54(1):8–29. - PubMed
    1. Braakhuis BJ, Tabor MP, Kummer JA, Leemans CR, Brakenhoff RH. A genetic explanation of Slaughter’s concept of field cancerization: evidence and clinical implications. Cancer Res. 2003;63(8):1727–30. - PubMed
    1. Robinson E, Neugut AI, Murray T, Rennart G. A comparison of the clinical characteristics of first and second primary head and neck cancers. A population-based study. Cancer. 1991;68(1):189–92. - PubMed
    1. Tsao M-S, Sakurada A, Cutz J-C, Zhu C-Q, Kamel-Reid S, et al. Erlotinib in lung cancer – Molecular and clinical predictors of outcome. New Engl J Med. 2005;353(2):133–44. - PubMed

Publication types

Grants and funding