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Renal disease as a potential compounding factor in carcinogenesis experiments with Cd151-null mice

Oncogene volume 32, page 4457 (2013)Cite this article

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Li et al.1 recently described two-stage skin carcinogenesis experiments using wild-type and Cd151-null mice, showing that Cd151 deletion retarded tumorigenesis. Because this skin carcinogenesis model is highly sensitive to the mouse strain used, they backcrossed Cd151-null mice from 129Sv onto the FVB/N strain for four generations for these experiments. They state that further backcross was not carried out to avoid kidney pathology that occurs in FVB/N Cd151-null mice, and that the mice used for experiments had no obvious kidney defects. Two groups have independently described kidney pathology developing in FVB/N Cd151-null mice. Sachs et al.2 first reported proteinuria and histological abnormalities in CD151-null mice on a 129-FVB/N-mixed background, apparently arising quite early in the process of backcross onto the FVB/N strain and developing proteinuria before 3 weeks of age. Our group backcrossed the original C57BL/6 Cd151-null mice3 onto the FVB/N strain for 10 generations. When homozygous Cd151-null mice on this strain were bred, they showed proteinuria by 5 days of age and progressive kidney abnormalities, often leading to end-stage renal disease after 4 months of age.4 Because four generations of backcross carried out by Li et al. would be expected to result in mice homozygous for FVB/N alleles, randomly, at 87.5% of loci (assuming the first generation is the F1 cross), it is surprising that no kidney abnormality was observed over the course of their experiments.

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References

  1. Li Q, Yang XH, Xu F, Sharma C, Wang HX, Knoblich K et al. Tetraspanin CD151 plays a key role in skin squamous cell carcinoma. Oncogene 2013; 32: 1772–1783.

    Article  CAS  Google Scholar 

  2. Sachs N, Kreft M, van den Bergh Weerman MA, Beynon AJ, Peters TA, Weening JJ et al. Kidney failure in mice lacking the tetraspanin CD151. J Cell Biol 2006; 175: 33–39.

    Article  CAS  Google Scholar 

  3. Wright MD, Geary SM, Fitter S, Moseley GW, Lau LM, Sheng KC et al. Characterization of mice lacking the tetraspanin superfamily member CD151. Mol Cell Biol 2004; 24: 5978–5988.

    Article  CAS  Google Scholar 

  4. Baleato RM, Guthrie PL, Gubler MC, Ashman LK, Roselli S . Deletion of CD151 results in a strain-dependent glomerular disease due to severe alterations of the glomerular basement membrane. Am J Pathol 2008; 173: 927–937.

    Article  CAS  Google Scholar 

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Acknowledgements

I thank Ms Crystal Naudin for permission to present her unpublished data.

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  1. School of Biomedical Sciences and Pharmacy, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia

    L K Ashman

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  1. L K Ashman
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Correspondence to L K Ashman.

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Ashman, L. Renal disease as a potential compounding factor in carcinogenesis experiments with Cd151-null mice. Oncogene 32, 4457 (2013). https://doi.org/10.1038/onc.2013.73

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