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Animal Models |
From the Department of Veterinary Biosciences and Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio
Papillary thyroid carcinomas in humans are associated with the
ret/PTC oncogene and, following loss of p53
function, may progress to anaplastic carcinomas. Mice with
thyroid-targeted expression of ret/PTC1 developed
papillary thyroid carcinomas that were minimally invasive and did not
metastasize. These mice were crossed with p53-/- mice to investigate
whether loss of p53 would promote anaplasia and metastasis of
ret/PTC1-induced thyroid tumors. The majority of
p53-/- mice died or were euthanized by 17 weeks of age due to the
development of thymic lymphomas, soft tissue sarcomas,
and testicular teratomas. All ret/PTC1 mice developed
thyroid carcinomas, but tumors in p53-/- mice were more
anaplastic, larger in diameter, more invasive,
and had a higher mitotic index than tumors in p53+/+ and p53+/- mice.
Thyroid tumors did not metastasize in any of the experimental p53+/+
and p53+/- mice 
28 weeks of age or p53-/- mice 17 weeks of
age; however, an older (170-day-old) male p53-/- mouse
used to maintain the colony developed anaplastic thyroid
carcinoma with liver metastases. These findings demonstrate that the
lack of functional p53 in ret/PTC1 mice promotes
anaplasia and invasiveness of thyroid carcinomas.
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