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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Castration

 
 
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Disease relevance of Castration

 

Psychiatry related information on Castration

 

High impact information on Castration

 

Chemical compound and disease context of Castration

 

Biological context of Castration

 

Anatomical context of Castration

 

Associations of Castration with chemical compounds

  • One grew in an androgen-independent fashion, whereas the second formed tumors that regressed following castration then regrew [31].
  • In the brain, this enzymatic system is not regulated by castration or sex steroid administration; furthermore, neural inputs seem to be ineffective at the hypothalamic level [32].
  • Follicle-stimulating hormone (FSH) beta, luteinizing hormone (LH) beta, and alpha subunit messenger RNA (mRNA) levels were examined in rats after castration and sex-steroid replacement [33].
  • Castration did not significantly alter ethanol consumption in males, although treatment of castrated rats with dihydrotestosterone resulted in a significant inhibition of this parameter [34].
  • All patients were taking flutamide at the time of entry, and previous treatments with medical or surgical castration, flutamide, suramin, and hydrocortisone had failed in all of these patients [35].
 

Gene context of Castration

  • This potentiation is not due to a further inhibition in tumor VEGF levels induced by castration [36].
  • IGFBP-5 mRNA was not detectable in tumors from control animals, but levels increased 120-fold in tumors 3 days after castration [37].
  • Levels of SREBP cleavage-activating protein, a regulator of SREBP transcriptional activity, decreased after castration and increased significantly at androgen independence [38].
  • Castration had no significant effect on IGFBP-2 expression [37].
  • SREBP-1 68-kDa protein levels were maintained throughout progression, however, SREBP-2 68-kDa protein expression increased after castration and during progression (3-fold) [38].
 

Analytical, diagnostic and therapeutic context of Castration

  • Although the primary tumors regressed following oophorectomy, the growth of late generations of the transplantable lines was not affected by castration or by treatment with estrogens, androgens, and progesterone [39].
  • Adrenalectomy or castration of males led to 35 or 45% mean decreases of dopamine sulfotransferase levels, indicating adrenal and gonadal participation in control of dopamine sulfotransferase production [40].
  • Orchidectomy on day 1 resulted in an approximately 50% decrease in adult SDN-POA volume; however, the influence of the testes on their resulting SDN-POA volume was replaced affectively by the administration of 100 micrograms or 1 mg of TP on postnatal day 2 or by a testicular (but not ovarian) graft on the day of castration [41].
  • Northern blotting of RNA from tumors collected at various times after castration indicates a rapid induction of IGFBP-5 concomitant with apoptotic regression of tumors, as detected by Apoptag staining of tumor sections after castration [37].
  • In mice bearing TRPM-2-overexpressing LNCaP tumors, tumor volume and serum prostate-specific antigen increased two to three times faster after castration and paclitaxel treatment compared with mice bearing control tumors [42].

References

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