Analysis Tools
mortality/aging
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• median survival of about 6 months following tumor induction with tamoxifen
• tumor induced mice treated with the BRAF inhibitor PLX4720 show improved survival
• tumor induced mice treated with both the BRAF inhibitor PLX4720 and the selective MEK inhibitor PD0325901show prolonged survival
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neoplasm
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• tamoxifen treated mice exhibit accelerated progression from papillary thyroid carcinoma to poorly differentiated thyroid carcinoma and overt undifferentiated anaplastic thyroid carcinoma with highly pleomorphic, atypical cells with evidence of necrosis
• carcinoma in tamoxifen treated mice shows tracheal invasion and extrathyroidal extension
• marker analysis indicates that anaplastic thyroid carcinoma in tamoxifen treated mice originates from thyroid epithelium
• tumors from tamoxifen treated mice exhibit very slow initial growth upon induction but rapid tumor growth after a variable latency
• mice supplemented with L-thyroxine immediately following tamoxifen administration show suppressed TSH levels and develop anaplastic thyroid carcinoma with a similar latency as unsupplemented controls
• anaplastic thyroid carcinomas exhibit a gene expression profile of high-grade, undifferentiated carcinomas
• tumor induced mice treated with the BRAF inhibitor PLX4720 show improved survival and a decrease in contralateral papillary thyroid carcinomas, however no decrease in anaplastic thyroid carcinoma size is seen and tumors even grow larger
• tumor induced mice treated with both the BRAF inhibitor PLX4720 and the selective MEK inhibitor PD0325901 show complete regression of tumors and prolonged survival
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• 19% of tamoxifen treated mice exhibit lung metastases
• however, region lymph node metastases are not seen
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endocrine/exocrine glands
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• tamoxifen treated mice exhibit accelerated progression from papillary thyroid carcinoma to poorly differentiated thyroid carcinoma and overt undifferentiated anaplastic thyroid carcinoma with highly pleomorphic, atypical cells with evidence of necrosis
• carcinoma in tamoxifen treated mice shows tracheal invasion and extrathyroidal extension
• marker analysis indicates that anaplastic thyroid carcinoma in tamoxifen treated mice originates from thyroid epithelium
• tumors from tamoxifen treated mice exhibit very slow initial growth upon induction but rapid tumor growth after a variable latency
• mice supplemented with L-thyroxine immediately following tamoxifen administration show suppressed TSH levels and develop anaplastic thyroid carcinoma with a similar latency as unsupplemented controls
• anaplastic thyroid carcinomas exhibit a gene expression profile of high-grade, undifferentiated carcinomas
• tumor induced mice treated with the BRAF inhibitor PLX4720 show improved survival and a decrease in contralateral papillary thyroid carcinomas, however no decrease in anaplastic thyroid carcinoma size is seen and tumors even grow larger
• tumor induced mice treated with both the BRAF inhibitor PLX4720 and the selective MEK inhibitor PD0325901 show complete regression of tumors and prolonged survival
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homeostasis/metabolism
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• small increase in TSH levels (less than 10-fold elevation) in tamoxifen treated mice
• mice supplemented with L-thyroxine immediately following tamoxifen administration show suppressed TSH levels
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respiratory system
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• tamoxifen treated mice quickly deteriorate after progression to anaplastic thyroid carcinoma, with rapidly growing neck masses and development of audible respiratory stridor
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