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Apalutamide in the treatment of non-metastatic castration-resistant prostate cancer in an elderly patient with multiple comorbidities

100%
Liśkiewicz K.
OncoReview
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2023
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vol. 13
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issue 1
9-12
EN
Prostate cancer has been the most common malignant tumor in men in Poland since 2016 and is the second cause of death in this group of patients. The basic method of treatment in patients with advanced prostate cancer is androgen deprivation therapy, however, over time, the tumor evolves into a castration-resistant form, which poses a significant threat to the patient's life. This article presents a case of an elderly patient with internal diseases, who in the castration-resistant stage, was treated with a new generation androgen receptor blocker – apalutamide – in the first line of systemic treatment.
2
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Androgen receptor and c-Myc transcription factors as putative partners in the in vivo cross-talk between androgen receptor-mediated and c-Met-mediated signalling pathways

100%
Dudkowska M., Jaworski T., Grzelakowska-Sztabert B., Manteuffel-Cymborowska M.
Acta Biochimica Polonica
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2007
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vol. 54
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issue 2
253-259
EN
Cross-talk between two signal transduction pathways leads to a negative regulation of androgen-induced ornithine decarboxylase (ODC) gene expression in the mouse kidney. One pathway is triggered by testosterone via the intracellular androgen receptor, AR, and the other is induced by antifolate CB 3717 or folate via hepatocyte growth factor and its cell membrane receptor c-Met. Here we report the studies of the expression of AR and c-Myc transcription factors involved in ODC transactivation. Administration of CB 3717 or folate decreased the expression of AR. In contrast, testosterone did not modify AR mRNA content but augmented the AR protein. Furthermore, we demonstrate that administration of folate, but not testosterone, increases c-Myc transcript and protein level. We also document that activation of both examined pathways does not decrease the testosterone-induced AR protein level, but markedly increases c-Myc protein which is nearly 2-fold up-regulated compared to its level evoked solely by testosterone. We suspect that this pronounced increase of c-Myc protein might have functional consequences mirrored by down-regulated expression of AR target genes, among them ODC.
3
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The expression of androgen receptor in neurons of the anterior pelvic ganglion and celiac-superior mesenteric ganglion in the male pig

63%
Kaleczyc J., Kasica-Jarosz N., Pidsudko Z., Przyborowska A., Sienkiewicz W., Kaleczyc J., Kasica-Jarosz N., Pidsudko Z., Przyborowska A., Sienkiewicz W.
Polish Journal of Veterinary Sciences
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2019
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issue 1
4
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Osteoporoza po stosowaniu hormonalnej terapii antyandrogenowej raka gruczołu krokowego

51%
Cegieła U., Korzeniowska H., Wilk A.
Annales Academiae Medicae Silesiensis
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2012
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vol. 66
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issue 2
49-54
EN
Prostate cancer is a malicious tumor. Its development is determined by the lack of androgen equilibrium by the prostate. In pathogenesis of this disease, the androgen receptors also play an essential role. Androgen receptors activation in neoplastic cells leads to their diff erentiation and tumorous progression. Hormonal antiandrogenic therapy is the basic method of prostate cancer treatment, which induces decreased testosterone levels and/or inhibits the eff ect of androgen on androgen receptors. Orchidectomy or the administration of analogs or antagonists of gonadotropin- releasing hormone are used in order to decrease testosterone levels, whereas antiandrogens are administered in order to block androgen receptors. The decreased level of testosterone and the disorder in the function of androgen receptors lead to the impairment of bone cell function i.e. (osteoclasts, osteoblasts, osteocytes) and the development of osteoporosis in men. Androgens stimulate the proliferation, diff erentiation and activity of osteoblast. They stimulate the synthesis of bone matrix proteins and bone mineralization. They have proapoptotic eff ect on osteoclasts and antiapoptopic eff ect on osteoblasts and osteocytes. Androgens inhibit recruitment of osteoclasts and reduce bone resorption.
PL
Rak gruczołu krokowego jest nowotworem złośliwym. Jego rozwój jest determinowany brakiem równowagi androgenowej prostaty. W patogenezie choroby istotną rolę odgrywają także receptory androgenowe, których aktywacja w komórkach nowotworowych prowadzi do wzrostu ich różnicowania i progresji nowotworu. Podstawową metodą jego leczenia jest hormonalna terapia antyandrogenowa, polegająca na obniżeniu poziomu testosteronu lub zahamowaniu oddziaływania androgenów na receptory androgenowe. W celu obniżenia poziomu testosteronu stosuje się orchidektomię oraz terapię analogami lub antagonistami gonadoliberyny, natomiast w celu hamowania oddziaływania androgenów na receptory androgenowe stosuje się antyandrogeny. Zmniejszenie poziomu testosteronu i zaburzenia w funkcjonowaniu receptorów androgenowych prowadzą do upośledzenia funkcji komórek kostnych (osteoklastów, osteoblastów, osteocytów) i rozwoju osteoporozy u mężczyzn. Androgeny stymulują proliferację, różnicowanie i funkcje osteoblastów. Pobudzają syntezę białek macierzy kostnej i stymulują mineralizację. Wykazują efekt proapoptyczny na osteoklasty i antyapoptyczny na osteoblasty i osteocyty. Hamują rekrutację osteoklastów i zmniejszają resorpcję kości.
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