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© 1994 Oxford University Press

other

Activation of H-ras is prevalent in 1,3-butadiene-induced and spontaneously occurring murine Harderian gland tumors

T.L. Goodrow 1 5, W.W. Nichols 2, R.D. Storer 2, M.W. Anderson 3 and R.R. Maronpot 4

1Fox Chase Cancer Center Philadelphia, PA 19090
2Merck Research Laboratories West Point, PA 19486
3Cancer Research Institute, St Mary's Hospital and Medical Center Grand Junction, CO 81501
4NIEHS Research Triangle Park NC 27709, USA

5To whom correspondence should be addressed

Treatment of B6C3F1 mice with concentrations of 62.5–625 p.p.m. 1,3-butadiene by inhalation for up to 2 years causes a significantly increased incidence of Harderian gland (HG) neoplasms over untreated controls (Melnick,R.,Huff, J., Chou,B.J. and Miller,R.A. Cancer Res., 50, 6592–6599, 1990). Since a specific K-ras mutation (codon 13 GGC->CGC) had previously been described in lung and liver tumors from 1, 3-butadiene-treated B6C3F1 mice, we analyzed 23 adenomas and sis adenocarcinomas of the HG from mice exposed to 1,3-butadiene for this mutation and mutations in the H-ras gene. We also examined ras activation in 16 spontaneously occurring HG adenomas and one adenocarcinoma. DNA samples were prepared from paraffin-embedded tissues and analyzed by PCR followed by direct sequencing methods. Only one 1,3-butadiene-induced HG tumor contained the K-ras codon 13 mutation previously detected in lung and liver tumors. However, 16/29 HG tumors from the treated B6C3F1 mice contained H-ras codon 61 mutations. The mutations detected were: 12 CAA->CGA transitions, two CAA->CTA and two CAA->AAA transversions. Eleven of 17 spontaneous HG tumors contained mutations in H-ras codon 61: five CA->CGA transitions, two CAA->CTA transversions and four CAA->AAA transversions. While the spectrum of ras mutations did not differ between the spontaneously occurring and chemically induced tumors, these data indicate that activation of H-ras contributes to the process of HG tumorigenesis in both groups of these neoplasms.


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