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Expression of Retroviral Sequences and Oncogenes in Murine Hepatocellular Tumors¹

Cancer Center/Division of Environmental Sciences, Columbia University, New York, New York 10032 [T. A. D., S. G-C., I. B. W.], and Division of Experimental Oncology A, Istituto Nazionale per lo Studio e la Cura dei Tumori, 20133 Milan, Italy [G. M., G. D. P.]

The expression of endogenous retroviral sequences and of three cellular oncogenes was examined in three hepatocellular adenomas and in four carcinomas induced in male C57BL/6JDp x C3Hf/Dp F₁ (hereafter called B6C3F₁) mice by a single dose of nitrosodiethylamine, in five carcinomas that arose spontaneously in male C3Hf mice, and in the livers of normal age-matched control mice. In all of these adenomas and carcinomas, there was increased expression of Moloney murine leukemia virus- and intracisternal A particle-related sequences. The retrovirus-like VL30 sequence was expressed at significant levels in the normal liver of these mice and increased expression of this sequence was found in only 4 of the 12 tumors examined. Expression of endogenous mouse mammary tumor virus-related sequences was not detected in the normal livers or in any of the liver tumors. With respect to cellular oncogenes, increased expression of c-myc was seen in all of the B6C3F₁ tumors. Two of five normal liver samples and all of the tumors of the C3Hf mice displayed significant expression of c-myc. There was a slight increase in expression of c-Ha-ras in some of the tumors. Increased expression of c-fos was found in only 1 of the 12 tumors. Taken together, these studies indicate that both carcinogen-induced and spontaneous liver tumor formation in mice is associated with abnormalities in the expression of endogenous retrovirus-related DNA sequences and also specific cellular oncogenes.

¹ This investigation was partially supported by an Associazione Italiana per la Ricerca sul Cancro (A.I.R.C.) fellowship to T. A. Dragani, by a grant from the Finalized Project "Oncology," Consiglio Nazionale delle Ricerche (C.N.R.), Rome, Italy, and by a National Cancer Institute Grant 021111 and funding from the National Foundation for Cancer Research to I. B. Weinstein.

² To whom reprints for reports should be addressed.

Received 9/30/85. Revised 12/23/85. Accepted 12/30/85.

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