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Decreased hepatic nuclear L-triiodothyronine receptors in rats and mice bearing transplantable neoplasms.

The concentration of hepatic nuclear T3 receptors was measured in isolated nuclei from athyreotic mice bearing thyrotrophic tumors and intact rats with Walker 256 carcinoma. Receptor concentration was reduced in all tumor-bearing animals. The mean receptor capacity of the Walker tumor-bearing rats [0.31 +/- 0.05 (SEM) ng/mg DNA] was significantly decreased from simultaneously assayed controls (0.47 +/- 0.04 ng/mg DNA; P less than 0.01). No change in the apparent equilibrium association constant was observed. In individual rats, the magnitude of the decrease in nuclear T3 receptor concentration was highly correlated with the decrease in tumor-free body weight. Additional studies showed that the decrease in nuclear receptors was not due to delayed equilibration of added T3 with nuclear sites in vitro or to an increase in endogenous hepatic T3 concentration. The plasma concentration of total and free T4 and T3 was decreased in tumor-bearing rats. Plasma TSH concentration, however, remained unchanged. Thus, these transplantable neoplasms seem to be associated with decreased hepatic nuclear receptors and low concentrations of plasma thyroid hormones. The unchanged plasma TSH suggests that the animals remained euthyroid.

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[Establishment and characterization of human inflammatory breast carcinoma neoplasm transplantation in nude mice].

OBJECTIVE: To establish and characterize human inflammatory breast cancer xenograft in nude mice. METHODS: Animal studies, Northern and Western blot, zymograms and immunohistochemistry were used in our studies. RESULTS: Human transplantable inflammatory carcinoma were established in nude mice. This xenograft as its human counterpart exhibited striking erythema of the overlying skin, lympho-vascular invasion and other similar biological characteristics. It also exhibited lung metastasis 4-6 weeks after growth. This xenograft was ER, PR, Her-2/neu negative and p53, EGFR positive. Comparative studies of inflammatory breast cancer xenograft with non-inflammatory xenograft indicated 10-20 fold overexpression of E-cadherin and MUC1. CONCLUSIONS: This human inflammatory breast carcinoma xenograft will provide an excellent animal model to allow us to further dissect out both the upstream regulatory machinery and downstream effector molecules responsible for the inflammatory carcinoma phenotype.

Animals↗