Bulletin of Experimental Biology and Medicine

, Volume 120, Issue 4, pp 1046–1049 | Cite as

Alterations inc-myc, Ha-ras, andKi-ras protooncogenes in experimental rat mesothelioma

  • E. V. Kleimenova
  • G. Khoresovskii
  • L. A. Vasil'eva
  • M. G. Yakubovskaya
  • L. N. Pylev
Oncology
  • 24 Downloads

Abstract

Analysis of the polymorphism of restriction fragments or sequencing ofHa- andKi-ras gene segments containing codon 12 or 61, amplified in the polymerase chain reaction, failed to detect point mutations in any of seven rat mesothelioma cell lines or in 20 mesotheliomas induced in rats by erionite or chrysotile asbestos. These data indicate the absence ofras activation caused by point mutations in the “critical codons” in rat mesothelioma. A twofold increase in the content ofc-myc mRNA in 5 out of 8 examined tumors appears to reflect a more intensive proliferation of mesothelioma cells in comparison with normal mesothelium, but not their amplification. This is confirmed by the results of Southern blot-hybridization.

Key Words

ras and myc protooncogenes point mutations expression rat mesothelioma 

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References

  1. 1.
    L. N. Pylev,Vopr. Onkol.,20, No 4, 47–53 (1974).PubMedGoogle Scholar
  2. 2.
    L. N. Pylev, T. F. Kulagina, L. A. Vasil'eva,et al., Gig. Truda, No 6, 33 (1986).Google Scholar
  3. 3.
    I. Ausubel and M. Frederic,Current Protocols in Molecular Biology, New York (1990).Google Scholar
  4. 4.
    E. Bermudez, J. Everitt, and C. Walker,Exp. Cell Res.,190, 91 (1990).PubMedCrossRefGoogle Scholar
  5. 5.
    J. B. Bos,Cancer Res.,49, 4682 (1989).PubMedGoogle Scholar
  6. 6.
    J. Craighead, N. J. Akley, L. B. Gould, and B. L. Libbus,Amer. J. Pathol.,129, No 3, 448 (1987).Google Scholar
  7. 7.
    S. M. Kahn, W. Jiang, T. A. Culbertson,et al., oncogene, No 6, 1079 (1991).PubMedGoogle Scholar
  8. 8.
    H. Land, A. C. Chen, J. P. Morgenstern,et al., Mol. Cell. Biol., No 6, 1917 (1986).PubMedGoogle Scholar
  9. 9.
    R. A. Metcalf, J. A. Welsh, W. P. Bennett,et al., Cancer Res.,52, 2610 (1992).PubMedGoogle Scholar
  10. 10.
    R. R. Reddel, L. Malson-Shibley, B. I. Gerwin,et al., J. Nat. Cancer Inst.,81, 12 (1989).Google Scholar
  11. 11.
    F. Sanger, S. Nicklen, and A. R. Coulson,Proc. Nat. Acad. Sci. USA,74, 5463 (1977).PubMedCrossRefGoogle Scholar
  12. 12.
    R. A. Tubo and J. G. Rheinwald,Oncogene Res., No 1, 407 (1987).PubMedGoogle Scholar
  13. 13.
    C. Walker, J. Everitt, and J. C. Barrett,Amer. J. Ind. Med.,21, 253 (1992).Google Scholar

Copyright information

© Plenum Publishing Corporation 1996

Authors and Affiliations

  • E. V. Kleimenova
    • 1
  • G. Khoresovskii
    • 2
  • L. A. Vasil'eva
    • 1
  • M. G. Yakubovskaya
    • 1
  • L. N. Pylev
    • 1
  1. 1.Research Institute of CarcinogenesisCancer Research Center, Russian Academy of Medical SciencesMoscow
  2. 2.Institute of Chemical Industry ToxicologyUSA

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