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Ibrary Version eight.4 (June 2011).Effect of testosterone on thyroid cancer gene expression profileBecause we observed a striking difference in tumor size between the male mice with or with no castration, we focused our follow-up research on figuring out the mechanism by which male sex hormones (testosterone) could regulate thyroid cancer progression. To discover this, we performed genome-wide gene expression analysis on the thyroid cancer samples in the sham-surgery male and orchiectomized male mice and found distinctly various gene expression profiles among the two groups, which showed a total separation by sex hormone status (Figure 2A). Pathway analysis in the differentially expressed genes showed genes involved in immunity have been drastically overrepresented (Supplementary Table S1, obtainable at Carcinogenesis On the web). If these differentially expressed genes have been directly connected to male sex hormone, we reasoned that comparable alterations should also be observed when comparing thyroid cancer samples in the sham-surgery male mice to those from the oophorectomized female mice who also had no sex hormone(s). Indeed, comparable differentially expressed genes and pathways had been revealed by the gene expression profile comparison of cancer samples in between sham-surgery males and oophorectomized female mice (Figure 2B and C; Supplementary Tables S1 four, obtainable at Carcinogenesis On the web). In addition, a lot of the major differentially expressed genes between the sham-surgery male mice as well as the castrated male or female mice include testosterone receptor binding internet sites (Figure 2C). This suggests that the variations in gene expression profiles and pathways identified in the thyroid cancer samples were distinct for the sex hormone status in the mice. When the distinction in thyroid cancer progression was due to sex hormones, we subsequent postulated that removing sex organs in mice must get rid of this difference. Indeed, no difference was observed by comparing thyroid cancer tumor size/weight from the castrated male and female mice (Figure 2D). Even more striking, the gene expression profile comparison in the thyroid cancer samples from these mice revealed that only two genes have been differentially expressed (with 1.5-fold difference) excluding Xor Y-linked genes (Figure 2E). These data additional supported our hypothesis that the observed cancer sample gene expression differences in between sham-surgery male mice versus castrated male or female mice were straight because of endogenous male sex hormone (testosterone), as a result suggesting that testosterone plays a part in thyroid cancer progression in ThrbPV/PV mice.ResultsEffect of sex hormones on thyroid cancer initiation and progression in ThrbPV/PV miceThrbPV/PV mice spontaneously develop FTC in a pattern equivalent to IL-11 Proteins site humans (12), we therefore tested the idea that these mice could possibly be applied as a model method to study the effect of sex hormones on thyroid cancer initiation and progression. The rate and extent of thyroid cancer in 23 ThrbPV/PV mice, 54 months old, were evaluated by sex. Each male and female mice created thyroid cancer with histopathology showing capsular invasion, IL-32 Proteins Gene ID vascular invasion and anaplasia. There was a substantially higher price of distant metastasis in male mice compared with female (45 versus 17 , P 0.05), with 7 of 23 ThrbPV/PV mice developing distant metastases (7 with lung metastases, 2 also had heart metastases). To establish the effect of sex hormones on thyroid cancer initiation and progression, we.