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3β-diol can be a precursor of DHT in prostate cancer cells.

serum 3α-diol G levels reflect the androgen milieu in localized prostate cancer patients receiving ADT

A few studies reported that 3β-diol is a potential ligand of estrogen receptor β (ERβ) and has an antiproliferative effect

our results revealed that 3β-diol is potentially a precursor of DHT in prostate cancer cells

Bauman et al. showed that 3α-diol is inactive at AR, but induces prostate growth

Prostate cancer cells promoted synthesis from the DHT metabolite 3α-diol during the long duration of ADT

verified the synthesis of DHT from 3α- or 3β-diol via different pathways in prostate cancer cells in this study

HSD17B6 expression levels in prostate cancer can be useful for the diagnosis of high-risk prostate cancer

serum 3α-diol G levels reflect the adrenal androgen milieu in localized prostate cancer patients

3α- and 3β-diol has a much more significant role in intratumoral androgen metabolism during ADT

The risk of developing PC seems to be related to the diet

In the human prostate, ERβ is expressed in the basal epithelial cells and AR in the luminal epithelium.

For many years, DHT was considered to be the main hormone guiding prostate development and function. However, the idea was challenged when in 2001 Mahendroo et al. showed that mice in which both forms of 5α-reductase had been inactivated, have a normal functional prostate [50]. The question was then raised as to what is the real function of DHT in the prostate. In 1989 we hypothesized that DHT is a precursor of an oestrogen, 5α-androstane-3β,17β-diol (3β-Adiol) and that physiological levels of an oestrogen could be produced in the total absence of aromatase [51]. We later demonstrated that 3β-Adiol is abundant in the prostate and is a good natural ligand for ERβ

The overall effect of oestrogens in the immune system is determined by a balance between ERα and ERβ signalling

The hypothesis of our group is that ERβ plays an important role in regulating the differentiation of pluripotent haematopoietic progenitor cells whereas ERα induces proliferation

In tissues and cell lines of mammary epithelium for example, it has been noticed that E2 in the presence of ERα elicits proliferation, but in the presence of ERβ it inhibits proliferation

ERα and ERβ have distinctive tissue distributions and to the great surprise of endocrinologists [7] many tissues previously thought to be ‘oestrogen-insensitive tissues’ were found to be ERβ positive and oestrogen sensitive. The most notable of the ERα-negative ERβ-abundant tissues were the epithelium of the rodent ventral prostate [8], the granulosa cells of the ovaries [9] and the parenchyma of the lungs

female gender may predict greater tic severity in adulthood

male gender is a major risk factor for TS (with a male:female prevalence ratio estimated at ~4:1)

the typical age of onset coincides with adrenarche (6–7 years old); symptoms increase in severity until the beginning of puberty (12 years old) and then undergo a spontaneous amelioration, which becomes apparent with the end of puberty (at 18–19 years of age)

TS is diagnosed later in females than males

ample evidence supports the involvement of DAergic dysfunctions in TS

a number of clinical observations showed that tics in TS patients could be exacerbated by anabolic androgens

steroidogenic enzymes and androgen receptors may serve as putative therapeutic targets for this disorder

Unlike males, tic severity is typically increased after puberty in females

26% of females were found to experience exacerbation of tics in the estrogenic phase of the menstrual cycle, and this phenomenon was found to be correlated with increased tic severity at menarche

biochemical hallmark of adrenarche is the acquisition of 17,20 lyase activity by cytochrome P450 C17 (CYP17A1)

increased synthesis of dehydroepiandrosterone (DHEA) and androstenedione, which leads to the growth of axillary and pubic hair as well as enhancement in the oiliness of the skin