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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ALVA-41 cell line was derived from a bony metastasis from a human prostatic carcinoma. The line has a number of distinct, advantageous properties that should make it useful as a tool for the study of prostate cancer. It grows rapidly and is easy to work with. It has receptors for androgens and glucocorticoids but not for estrogens. Its growth is enhanced by physiological concentrations of dihydrotestosterone. It does not secrete prostate specific antigen, but does secrete prostatic acid phosphatase. Further, the secretion of prostatic acid phosphatase is enhanced by dihydrotestosterone.
Steroids 1994 Oct
PMID:Characterization of ALVA-41 cells, a new human prostatic cancer cell line. 753 40

In the present study, we investigated the effects of a steroid 5 alpha-reductase inhibitor, finasteride, when given orally (5 mg/day), on the serum levels of gonadal, hypophyseal, and adrenal hormones and the clinical significance of these effects. Forty-eight patients with a mean age of 63 (range 49-81) were included in the study. All patients had symptoms of benign prostatic hyperplasia. Serum levels of testosterone, dihydrotestosterone, follicle-stimulating hormone (FSH) luteinizing hormone (LH), prolactin, aldosterone, cortisol, and dehydroepiandrosterone were determined before the study. The degree of symptoms in each patient and serum prostate specific antigen levels were determined together with uroflowmetric studies. Sexual status of the patients was also assessed with a self-administered questionnaire. All patients received finasteride, 5 mg/day, for 6 weeks. All of the above mentioned studies were repeated at month 3 and month 6. All of the patients had baseline hormonal values within the normal range. At month 3, the dihydrotestosterone level decreased by 60%, while the testosterone level increased by 15%. FSH and LH levels decreased by 24% and 16%, respectively. The changes in the serum levels of these hormones were further evident at month 6. No significant changes were noted in the serum levels of prolactin, aldosterone, cortisol, and dehydroepiandrosterone. Thirty-six patients (75%) were judged to be potent before the treatment. Finasteride caused erectile dysfunction in 8 patients (22%) by month 3 and in 12 (33%) by month 6. A substantial improvement was noted in symptoms of benign prostatic hyperplasia in all patients. The serum prostate specific antigen level decreased by 42% and 50% at month 3 and at month 6, respectively. Continued administration of finasteride, 5 mg/day alters the serum levels of testosterone, dihydrotestosterone, FSH, and LH significantly. Finasteride also causes sexual dysfunction in a substantial number of patients and should be offered with caution to patients who have an active sexual life.
Steroids 1998 Apr
PMID:Effects of the 5 alpha-reductase inhibitor finasteride on serum levels of gonadal, adrenal, and hypophyseal hormones and its clinical significance: a prospective clinical study. 958 55

Androgen receptor (AR) and kallikrein (KLK-2) regulates the PSA (prostate specific antigen) transcription and activation, respectively. We investigated the individual and combined risk of KLK-2, PSA and AR gene polymorphism in histologically confirmed CaP patients and healthy controls from north India. DNA was extracted from peripheral blood leucocytes pellet of 277 subjects. AR repeats analysis was done by PCR-Genscan method. PSA and KLK-2 were genotyped by PCR-RFLP method. Kruskal-Wallis test and logistic regression was applied for mean comparison and risk determination. A significant association for CaP risk was observed with short AR-CAG repeats (OR=3.36, p<0.001) and CC genotype of KLK-2 (OR=2.78, p=0.031), however, no association was found with PSA and AR-GGN repeat polymorphism. PSA/GG genotype was significantly associated with higher Gleason score (> or =7) of tumor (OR=6.23, p<0.01). No association was observed with other confounding variables such as PSA and age with any of these polymorphisms. Thus, we hypothesize that these polymorphisms may influence the etiology of CaP and may have the probability to become appropriate marker either independently or in combination. The combined information on serum PSA level, PSA (G/A), KLK-2 (C/T) genotypes and AR (CAG; GGN repeat) may assist in the deterrence of unnecessary biopsies.
Steroids 2007 Apr
PMID:Is there an inter-relationship between prostate specific antigen, kallikrein-2 and androgen receptor gene polymorphisms with risk of prostate cancer in north Indian population? 1725 35

Here, the synthesis and the evaluation of novel 20-aminosteroids on androgen receptor (AR) activity is reported. Compounds 11 and 18 of the series inhibit both the wild type and the T877A mutant AR-mediated transactivation indicating AR antagonistic function. Interestingly, minor structural changes such as stereoisomers of the amino lactame moiety exhibit preferences for antagonism among wild type and mutant AR. Other tested nuclear receptors are only weakly or not affected. In line with this, the prostate cancer cell growth of androgen-dependent but not of cancer cells lacking expression of the AR is inhibited. Further, the expression of the prostate specific antigen used as a diagnostic marker is also repressed. Finally steroid 18 enhances cellular senescence that might explain in part the growth inhibition mediated by this derivative. Steroids 11 and 18 are the first steroids that act as complete AR antagonists and exhibit AR specificity.
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PMID:20-Aminosteroids as a novel class of selective and complete androgen receptor antagonists and inhibitors of prostate cancer cell growth. 2082 91

The skin irritating principle from Thapsia garganica was isolated, named thapsigargin and the structure elucidated. By inhibiting the sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA) thapsigargin provokes apoptosis in almost all cells. By conjugating thapsigargin to peptides, which are only substrates for either prostate specific antigen (PSA) or prostate specific membrane antigen (PSMA) prodrugs were created, which selectively affect prostate cancer cells or neovascular tissue in tumors. One of the prodrug is currently tested in clinical phase II. The prodrug under clinical trial has been named mipsagargin.
Steroids 2015 May
PMID:Targeting thapsigargin towards tumors. 2506 87