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© 1993 Oxford University Press

other

C57BL/6 mice are resistant to tumor promotion by full thickness skin wounding

J. DiGiovanni 1, T. S.Bhatt and S. E.Walker

Department of Carcinogenesis, The University of Texas, M.D.Anderson Cancer Center, Science Park—Research Division PO Box 389, Smithville, TX 78957, USA

1To whom correspondence should be addressed

The present study demonstrates that C57BL/6 mice, previously shown to be relatively resistant to skin tumor promotion by phorbol esters as well as several other classes of tumor promoters, are resistant to skin tumor promotion by full thickness skin wounding. Two separate experiments were performed comparing female SENCAR and C57BL/6 mice for their sensitivity to skin tumor promotion by skin wounding following initiation with 7,12-dimethylbenz[a]-anthracene (DMBA). In the first experiment, groups of mice were initiated with 25 nmol DMBA and then received full thickness skin wounds in the initiated skin 2 weeks later. Neither SENCAR nor C57BL/6 mice developed skin tumors during the 26 weeks following initial wounding. However, these groups were rewounded in week 27 and 14 weeks later the SENCAR mice had developed a significant tumor response (0.75 papillomas per mouse, 55% incidence). At this time, the C57BL/6 mice still did not have a tumor response significantly different from the acetone-initiated controls. A second experiment was performed using a 100 nmol initiating dose of DMBA. Fifteen weeks after initial wounding in this experiment, the group of SENCAR mice had 0.76 papillomas per mouse (41% incidence) whereas no tumors were present in the group of C57BL/6 mice, even 31 weeks after the initial wounding. The results demonstrate that C57BL/6 mice are resistant to an endogenous skin tumor promotion mechanism and strongly support a link between skin tumor promotion by several classes of chemical promoters and full thickness wounding.


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