Mutationally activated K-ras 4A and 4B both mediate lung carcinogenesis

Charles E. Patek, Mark J. Arends, William A.H. Wallace, Feijun Luo, Suzanne Hagan, David G. Brownstein, Lorraine Rose, Paul S. Devenney, Walter Kolch, Owen J. Sansom

Research output: Contribution to journalArticle

Abstract

To examine the roles of endogenous K-ras 4A and K-ras 4B splice variants in tumorigenesis, murine lung carcinogenesis was induced by N-methyl-N-nitrosourea (MNU), which causes a K-ras mutation (G12D) that jointly affects both isoforms. Compared with age-matched K-rastm¿4A/- mice (where tumours can express mutationally activated K-ras 4B only), tumour number and size were significantly higher in K-ras+/- mice (where tumours can also express mutationally activated K-ras 4A), and significantly lower in K-rastm¿4A/tm¿4A mice (where tumours can express both wild-type and activated K-ras 4B).

Original languageEnglish
Pages (from-to)1105-1114
Number of pages10
JournalExperimental Cell Research
Volume314
Issue number5
DOIs
Publication statusPublished - 1 Mar 2008

Keywords

  • K-ras 4B
  • lung cancer
  • K-ras 4A
  • tumorigenesis

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    Patek, C. E., Arends, M. J., Wallace, W. A. H., Luo, F., Hagan, S., Brownstein, D. G., Rose, L., Devenney, P. S., Kolch, W., & Sansom, O. J. (2008). Mutationally activated K-ras 4A and 4B both mediate lung carcinogenesis. Experimental Cell Research, 314(5), 1105-1114. https://doi.org/10.1016/j.yexcr.2007.11.004