Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Original Paper
  • Published:

L552S, an alternatively spliced isoform of XAGE-1, is over-expressed in lung adenocarcinoma

Oncogene volume 20, pages 7699–7709 (2001)Cite this article

Abstract

Using a combination of cDNA subtraction and microarray analysis, we report here the identification and characterization of L552S, an over-expressed, alternatively spliced isoform of XAGE-1 in lung adenocarcinoma. Real-time RT–PCR analysis shows that L552S is expressed at levels greater than 10-fold in 12 of 25 lung adenocarcinoma tumors compared with the highest expression level found in all normal tissues tested. L552S is expressed in both early and late stages of lung adenocarcinoma, but it was not detected in large cell carcinoma, small cell carcinoma, or atypical lung neuroendocrine carcinoid. The full-length cDNA for L552S comprises 770 bp and encodes a polypeptide of 160 amino acids. C-terminal 94 amino acids of L552S are identical to a cancer testis antigen, XAGE-1, found in Ewing's sarcoma. Genomic sequence analysis has revealed that L552S and XAGE-1 are alternatively spliced isoforms, and expression of both L552S and XAGE-1 isoforms are present in lung adenocarcinoma. Immunohistochemistry analysis using affinity purified L552S polyclonal antibodies demonstrated specific nuclear staining in 10 of 12 lung adenocarcinoma samples. Furthermore, antibody responses to recombinant L552S protein were observed in seven of 17 lung pleural effusion fluids of lung cancer patients. These results strongly imply that L552S protein is immunogenic and suggest that it might have use as a vaccine target for lung cancer.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1
Figure 4
Figure 2
Figure 3
Figure 5
Figure 6
Figure 7
Figure 8
Figure 9

Similar content being viewed by others

References

  • Boel P, Wildmann C, Sensi ML, Brasseur R, Renauld JC, Coulie P, Boon T, van der Bruggen P . 1995 Immunity 2: 167–175

  • Brinckerhoff LH, Thompson LW, Slingluff Jr CL . 2000 Curr. Opin. Oncol. 12: 163–173

  • Brinkmann U, Vasmatzis G, Lee B, Pastan I . 1999 Cancer Res. 59: 1445–1448

  • Chen YT, Gure AO, Tsang S, Stockert E, Jager E, Knuth A, Old LJ . 1998 Proc. Natl. Acad. Sci. USA 95: 6919–6923

  • Chen YT, Old LJ . 1999 Cancer. J. Sci. Am. 5: 16–17

  • Heng HH, Squire J, Tsui LC . 1992 Proc. Natl. Acad. Sci. USA 89: 9509–9513

  • Heng HH, Tsui LC . 1993 Chromosoma 102: 325–332

  • Jungbluth AA, Stockert E, Chen YT, Kolb D, Iversen K, Coplan K, Williamson B, Altorki N, Busam KJ, Old LJ . 2000 Br. J. Cancer 83: 493–497

  • Liu XF, Helman LJ, Yeung C, Bera TK, Lee B, Pastan I . 2000 Cancer Res. 60: 4752–4755

  • Martelange V, De Smet C, De Plaen E, Lurquin C, Boon T . 2000 Cancer Res. 60: 3848–3855

  • Robbins PF, Kawakami Y . 1996 Curr. Opin. Immunol. 8: 628–636

  • Tureci O, Sahin U, Schobert I, Koslowski M, Scmitt H, Schild HJ, Stenner F, Seitz G, Rammensee HG, Pfreundschuh M . 1996 Cancer Res. 56: 4766–4772

  • Tureci O, Sahin U, Zwick C, Koslowski M, Seitz G, Pfreundschuh M . 1998 Proc. Natl. Acad. Sci. USA 95: 5211–5216

  • Van den Eynde B, Peeters O, De Backer O, Gaugler B, Lucas S, Boon T . 1995 J. Exp. Med. 182: 689–698

  • van der Bruggen P, Traversari C, Chomez P, Lurquin C, De Plaen E, Van den Eynde B, Knuth A, Boon T . 1991 Science 254: 1643–1647

  • Wang T, Hopkins D, Schmidt C, Silva S, Houghton R, Takita H, Repasky E, Reed SG . 2000 Oncogene 19: 1519–1528

  • Yoshimatsu T, Yoshino I, Ohgami A, Takenoyama M, Hanagiri T, Nomoto K, Yasumoto K . 1998 J. Surg. Oncol. 67: 126–129

Download references

Acknowledgements

We would like to thank Qualtek for their expert IHC analysis. We also thank Dr Martin A Cheever for his critical reading of this manuscript.

Author information

Authors and Affiliations

  1. Department of Tumor Antigen Discovery, Corixa Corporation, 1124 Columbia Street, Seattle, WA 98104, Washington, USA

    Tongtong Wang, Liqun Fan, Yoshihiro Watanabe, Patricia McNeill, Gary R Fanger, David H Persing & Steven G Reed

  2. Department of Pathobiology, University of Washington, Seattle, WA 98195, Washington, USA

    Steven G Reed

Authors
  1. Tongtong Wang
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Liqun Fan
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Yoshihiro Watanabe
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Patricia McNeill
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Gary R Fanger
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. David H Persing
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Steven G Reed
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Tongtong Wang.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Wang, T., Fan, L., Watanabe, Y. et al. L552S, an alternatively spliced isoform of XAGE-1, is over-expressed in lung adenocarcinoma. Oncogene 20, 7699–7709 (2001). https://doi.org/10.1038/sj.onc.1204939

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/sj.onc.1204939

Keywords

This article is cited by

Search

Advanced search

Quick links