Ecdysone were detected in the majority of CRPC

Els are the driving forces Kr The CRPC. Ecdysone The gene for prostate-specific antigen gene is sensitive to androgens and PSA protein levels were detected in the majority of CRPC what. A functional AR signaling Several authors have found that there. Several mechanisms responsible for the castration resistance There are five main mechanisms AR ultimately, the F Promotion of cell growth s functions. The androgen receptor is amplified in 30% of the 25 tumors, castration. AR erh Hte lead to an increased FITTINGS sensitivity to small residual amounts of androgens produced by the adrenal gland. Zus Tzlich in some cases F There is evidence of increased Hte rate of conversion T DHT by the enzyme 5-reductase. May, moreover, the AR gene itself mutated are to be mistaken for a mutant protein may k Ie stero by other hormones Circulating and metabolism are activated.
Selumetinib By product and androgen antagonists such as flutamide These include the expression of isoforms of low molecular weight lack the AR Ligandenbindedom Ne and constitutively active, in order to makes the AR function in the absence of androgens Aligned. Cooperation in the regulation of the expression or corepressor loss can also relieved. The conversion of androgens to anti-androgen agonists or erm Equalized constitutive activation of the AR, in spite of the absence of significant amounts of androgens traffic Constitutive activation of AR may also from the phosphorylation of AR by various effectors that makes for a configuration Change in the AR Aligned to erh from her FITTINGS Transkriptionsaktivit t and transcription of target genes in CRPC cells carry rate of the castration cells sensitive ver changed.
Au Addition ver MODIFIED expression of co-repressor and binding and / or AR-phosphorylation also, ver the binding profiles of AR in CRPC cells Changed as compared to its binding to cells sensitive to castration. It is interesting to note that most cells castration resistant prostate cancer are still sensitive to androgens. Although these cells continue to be treated with anti-androgens cro when they proliferate with an h Higher speed than by zus USEFUL doses of androgens challenged. Expression of RA is also responsible for the survival of the cell and in many cases Cases it has been found there the loss of the AR expression leads to cell death, even in CRPC cells.
It is therefore likely that the ligand-dependent-Dependent AR Transkriptionsaktivit t primarily responsible for the regulation of cell proliferation cycle is w During ligand independent Ngig AR activity T regulate k Can also cell survival. Therefore, removal of androgens entered dinner in cell cycle arrest, but also in the absence of ligand, the AR can independently by mechanisms Ngig of ligand binding, the cells are alive h Enabled lt. If other pathwaysthat regulate cell cycle activated in CRPC cells, it can lead dinner release of growth factors and tumor growth arrest re. 2.3. The activation of signaling pathways, the AR function in cells CRPC studies from different laboratories bypass indicate the existence of alternative paths in CRPC cells that avoid the need for the AR in the regulation of cell-cycle paths. Thus can be active AR and functional, but the survival of the cells can be controlled in parallel by proliferation

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