Bulletin of Experimental Biology and Medicine

, Volume 149, Issue 5, pp 615–620 | Cite as

Squamous Cell Carcinoma of the Esophagus: Evaluation of the Status of Epidermal Growth Factor Receptors (EGFR and HER-2) by Immunohistochemistry and in Situ Hybridization

  • V. V. Delektorskaya
  • G. Yu. Chemeris
  • L. E. Zavalishina
  • A. A. Ryazantseva
  • A. Yu. Grigorchuk
  • P. V. Kononets
  • M. I. Davydov
Oncology

We performed a parallel evaluation of the status of epidermal growth factor receptors EGFR and HER-2 in tumor samples from 31 patients with squamous cell carcinoma of the esophagus. Hyperexpression of proteins was detected by immunohistochemical methods and gene amplification and other chromosome abnormalities were studied using FISH reaction. Evaluation of EGFR status showed that amplification of EGFR gene was present in 25% cases and chromosome 7 polysomy was detected in 29.2% cases positive by protein expression (2+/3+). Immunohistochemically positive EGFR status was confirmed by the results of FISH reaction for gene amplification and chromosome 7 polysomy in 54.2% cases (p=0.002). During evaluation of HER-2 status in the tumor, hyperexpression of the protein detected histochemically was not confirmed by FISH reaction for detection of amplification of the corresponding gene in 16.1% cases. In 22.6% patients, chromosome 7 polysomy was detected; it was not accompanied by amplification of HER-2 gene, but was related to immunohistochemically positive status of the tumor. Hyperexpression of EGFR protein significantly correlated with the presence of intravascular invasion (p=0.006) and increased depth of invasion (p=0.044), while amplification of EGFR gene (≥2.2) correlated with low differentiation degree of the tumor (p=0.006). The outcome of the disease was not associated with EGFR status at the gene and protein levels, whereas clinical course of the disease in patients with immunohistochemically negative expression of HER-2 protein was more favorable than in patients with positive expression (p=0.004). The results of this study suggest that hyperexpression/amplification of EGFR and hyperexpression of HER-2 are important clinical markers for evaluation of disease prognosis and development of new regimens of targeted therapy for patients with squamous cells carcinoma of the esophagus.

Key Words

carcinoma of the esophagus immunohistochemistry fl uorescent in situ hybridization EGFR HER-2 

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References

  1. 1.
    V. V. Delektorskaya, G. Yu. Chemeris, P. V. Kononets, and A. Yu. Grigorchuk, Byull. Eksp. Biol. Med., 148, No. 8, 213–218 (2009).Google Scholar
  2. 2.
    M. Akamatsu, T. Matsumoto, K. Oka, et al., Int. J. Radiat. Oncol. Biol. Phys., 57, 1323–282 (2003).PubMedGoogle Scholar
  3. 3.
    M. Dreilich, A. Wanders, D. Brattström, et al., // Dis. Esophagus., 19, No. 4, 224–231 (2006).CrossRefPubMedGoogle Scholar
  4. 4.
    L. Gibault, J. P. Metges, V. Conan-Charlet, et al., Br. J. Cancer, 93, 107–115 (2005).CrossRefPubMedGoogle Scholar
  5. 5.
    I. Gockel, M. Moehler, K. Frerichs, et al., Oncol. Rep., 20, No. 4, 845–850 (2008).PubMedGoogle Scholar
  6. 6.
    M. Gotoh, H. Takiuchi, S. Kawabe, et al., Jpn. J. Clin. Oncol., Vol. 37, No. 9, 652–657 (2007).CrossRefPubMedGoogle Scholar
  7. 7.
    M. Hanawa, S. Suzuki, Y. Dobashi, et al., Int. J. Cancer., 118, 1173–1180 (2006).CrossRefPubMedGoogle Scholar
  8. 8.
    Z. Liang, X. Zeng, J. Gao, BMC Cancer, 8, 363 (2008).CrossRefPubMedGoogle Scholar
  9. 9.
    D. C. Lin, X. L. Du, M. R. Wang, Dis. Esophagus., 22, No. 1, 9–20 (2009).CrossRefPubMedGoogle Scholar
  10. 10.
    K. Mimura, K. Kono M., Hanawa, et al., Br. J. Cancer, 92, 1253–1260 (2005).CrossRefPubMedGoogle Scholar
  11. 11.
    S. Morgan and J. R .Grandis, Exp. Cell Res., 315, No. 4, 572–582 (2009).CrossRefPubMedGoogle Scholar
  12. 12.
    U. Reichelt, P. Duesedau, M. Tsourlakis, et al., Mod. Pathol., 20, 120–129 (2007).CrossRefPubMedGoogle Scholar
  13. 13.
    I. Rubin and Y. Yarden, Ann. Oncol., 12, Suppl. 1, S3–S8 (2001).CrossRefPubMedGoogle Scholar
  14. 14.
    Y. Sato-Kuwabara, J. I. Neves, J. H. Fregnani, et al., BMC Cancer., 9, 6 (2009).CrossRefPubMedGoogle Scholar
  15. 15.
    P. Sunpaweravong, S. Sunpaweravong, P. Puttawibul, et al., J. Cancer Res. Clin. Oncol., 131, 111–119 (2005).CrossRefPubMedGoogle Scholar

Copyright information

© Springer Science+Business Media, Inc. 2010

Authors and Affiliations

  • V. V. Delektorskaya
    • 1
  • G. Yu. Chemeris
    • 1
  • L. E. Zavalishina
    • 2
  • A. A. Ryazantseva
    • 2
  • A. Yu. Grigorchuk
    • 1
  • P. V. Kononets
    • 1
  • M. I. Davydov
    • 1
  1. 1.N. N. Blokhin Cancer Research CenterRussian Academy of Medical SciencesMoscowRussia
  2. 2.P. A. Gertsen Moscow Research Oncological InstituteFederal Agency for High-Technological Medical CareMoscowRussia

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