This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Becker, Frederick. F. Search for Related Content PubMed PubMed Citation Articles by Becker, Frederick. F.

Progression of Tumor Histiotype during Mouse Hepatocarcinogenesis Associated with the Viable Yellow (A^vy) Gene¹

Section of Experimental Pathology, The University of Texas M.D. Anderson Hospital and Tumor Institute at Houston, Houston, Texas 77030

Increasing attention has been focused recently upon those factors in carcinogenesis that are responsible for the proliferation of initiated cells and the increasingly aberrant phenotype that they progressively manifest. The agouti locus allele A^vy (viable yellow) has been shown to be associated with conditions which favor promotion of cells that have been initiated by a wide variety of causes, in many organs, but has not been previously associated with tumor progression in those systems. In the current study, the presence of the A^vy gene in a strain of mice not normally predisposed to hepatocarcinogenesis, C57BL/6N was, for the first time, associated not only with much earlier appearance, but with progression of the histiotype of hepatic tumors, following neonatal administration of diethylnitrosamine. At 52 weeks, 28 C57BL/6N mice demonstrated 7 mouse liver tumors 0.5 cm or greater in diameter, all of more benign histiotype, without associated metastasis. The 31 C57BL/6N-A^vy demonstrated 194 mouse liver tumors at that time, 22% of which were of malignant histiotype, 19% of which were associated with metastasis. This system would appear to offer the possibility of identifying the underlying mechanisms for components of the carcinogenic process.

In addition, the C57BL/6N-A^vy mouse appears to offer advantages as a test animal in bioassay procedures that use the liver as a target organ. Thus, it represents a mouse with little or no spontaneous predisposition to hepatocarcinogenesis, with a predicted short lag period toward response to hepatocarcinogens.

¹ The work was supported by funds received from NIH Grant CA20657 and the Sid W. Richardson Foundation.

Received 1/16/85. Revised 8/20/85. Revised 1/13/86. Accepted 1/20/86.

This article has been cited by other articles:

				V. Ablamunits, Y. Cohen, I. B. Brazee, H. P. Gaetz, C. Vinson, and S. Klebanov Susceptibility to Induced and Spontaneous Carcinogenesis Is Increased in Fatless A-ZIP/F-1 but not in Obese ob/ob Mice. Cancer Res., September 1, 2006; 66(17): 8897 - 8902. [Abstract] [Full Text] [PDF]