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ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Frederick, Maryland 21701 [N. S., R. S. P., Y. O., G. V. W.]; Ludwig Institute for Cancer Research, St. Mary's Hospital Medical School, London W2 1PG, United Kingdom [F. P.]; Department of Molecular Biology, Squibb Institute for Cancer Research, Princeton, New Jersey 08543 [M. P. R.]; National Cancer Institute, Navy Medical Oncology Branch, Naval Hospital, Bethesda, Maryland 20814 [R. I. L.]; and Pathology Associates, Inc., Frederick, Maryland 21701 [R. K.]
Transgenic mice carrying and expressing a mos protooncogene, linked to the Moloney murine sarcoma virus long terminal repeat, develop severe neurological defects and lens abnormalities. Here we report that after long latent periods, mice in three of four of these mos transgenic lines develop a high frequency of multicentric pheochromocytomas and/or medullary thyroid neoplasms. The pattern of tumor formation is remarkably similar to the human autosomal dominantly inherited neoplastic syndrome, multiple endocrine neoplasia type 2 (MEN 2), and tumors from these transgenic animals display the same neuroendocrine marker staining pattern as seen in MEN 2. The similarity between the tumor pathologies and presentation patterns of MEN 2 patients and mos transgenic mice suggests that they may arise through related pathways. The type of tumor presentation varies in a line-dependent manner indicating that there is interaction between the transgene and the genetic background. Moreover, when the non-tumor-bearing mos transgenic line is crossed to a different mouse background, the F1 offspring display the MEN 2 phenotype. These studies indicate that penetrance of the autosomal dominant mos transgenic phenotype is dependent on both integration site and background.
1 Research sponsored in part by the National Cancer Institute, Department of Health and Human Services, under Contract NO1-CO-74101 with ABL. The contents of this publication do not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the United States Government. By acceptance of this article, the publisher or recipient acknowledges the right of the United States Government and its contractors and agents to retain a nonexclusive, royalty-free license in and to any copyright covering the article.
Received 8/12/91. Accepted 10/30/91.
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