Validation of the Pitts unified theory of prostate cancer, late-onset hypogonadism and carcinoma: the role of steroid 5?-reductase and steroid aromatase
| Autor: | W. Reid Pitts |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Male
medicine.medical_specialty medicine.drug_class Urology Paracrine signalling Prostate cancer Aromatase Sex Factors 3-Oxo-5-alpha-Steroid 4-Dehydrogenase Prostate Neoplasms Internal medicine Humans Medicine Obesity Age of Onset skin and connective tissue diseases Autocrine signalling Testosterone biology Aromatase Inhibitors business.industry Hypogonadism Carcinoma Prostatic Neoplasms medicine.disease Androgen Dietary Fats medicine.anatomical_structure Endocrinology Dihydrotestosterone biology.protein Female business medicine.drug |
| Zdroj: | BJU International. 100:254-257 |
| ISSN: | 1464-410X 1464-4096 |
| DOI: | 10.1111/j.1464-410x.2007.06896.x |
| Popis: | Steroid 5AR converts testosterone to dihydrotestosterone; steroid aromatase converts testosterone to oestradiol in males and females (androgen deprivation results in oestrogen deprivation). Oestradiol, the product of testosterone aromatization, binds to the androgen and oestrogen receptors. Dihydrotestosterone (DHT) mediates cellular apoptosis through the paracrine prostate stromal cell factors and autocrine prostate epithelial cell factors (alopecia, remodelling of the anterior urethral plate, and remodelling of the embryonic prostate). Oestrogen mediates cellular proliferation through the paracrine and autocrine factors. Decreasing 5AR by 90% results in DHT decreasing by 35 times, testosterone increasing by 20 times, and oestrogen increasing by 19 times. The same changes are found in Gleason 4, 5 prostate cancer. Oestrogen plus testosterone increases the oestrogen proliferation by a factor of 100. Low 5AR results in unchecked prostatic epithelial cell proliferation from increased oestrogen without the apoptosis mediated by DHT (i.e. carcinogenesis) [18–20]. |
| Databáze: | OpenAIRE |
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