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Search results for: Androgen Receptor (Phospho-Ser650) Antibody

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#32742928   2020/06/02 To Up

Androgen receptor in bladder cancer: A promising therapeutic target.

There has been a significant progress in the treatment of metastatic urothelial carcinoma in the last few years with the advent of immunotherapy after a long gap of no drug approvals for over 4 decades. While immunotherapy with checkpoint inhibitors has revolutionized the treatment of urothelial carcinoma, unfortunately, only a minority of patients respond to immunotherapy. Treatment options for patients who do not respond and/or progress on immunotherapy are very limited and overall prognosis remains dismal in metastatic urothelial carcinoma. The first targeted therapy targeting the fibroblast growth factor receptor (FGFR) was recently approved for bladder cancer, but it is effective only in select patients harboring the FGFR2 and FGFR 3 mutations. Antibody drug conjugates like enfortumab vedotin have shown promising activity in clinical trials. Development of novel targeted therapies remains an area of investigation and an unmet need in bladder cancer. Exploitation of androgen receptor (AR) is a potential strategy for targeted drug development in bladder cancer. A significant proportion of urothelial carcinoma patients express AR irrespective of gender. AR signaling in urothelial carcinoma has been linked to progression through multiple mechanisms, including activation of human epidermal growth factor receptor-2 (EGFR or HER-2) signaling and epithelial to mesenchymal transition (EMT). Furthermore, AR is enriched in the luminal papillary mRNA subtype of urothelial carcinoma and also mediates resistance to cisplatin-based chemotherapy. Preclinical evidence suggests that AR inhibition can successfully inhibit urothelial carcinoma growth as monotherapy and is synergistic with cisplatin-based chemotherapy. We review the preclinical and clinical evidence supporting the putative role of AR signaling in urothelial carcinoma pathogenesis, progression and its role as a novel therapeutic target and future directions.
Abhishek Tripathi, Shilpa Gupta

2433 related Products with: Androgen receptor in bladder cancer: A promising therapeutic target.



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#32736705   2020/07/19 To Up

Ectodysplasin-A2 induces dickkopf 1 expression in human balding dermal papilla cells overexpressing the ectodysplasin A2 receptor.

Androgenetic alopecia (AGA) is a common genetic disorder, and a X-chromosomal locus that contains the androgen receptor (AR) and ectodysplasin A2 receptor (EDA2R) genes represents a major susceptibility locus for AGA. In our previous study, we reported that ectodysplasin-A2 (EDA-A2) induces apoptosis in cultured human hair follicle (HF) cells and promotes the regression of HFs in mice. However, the role of the EDA-A2/EDA2R in AGA remains unknown, as the causative gene in this pathway has not yet been identified and potential functional connections between EDA-A2 signaling and the androgen pathway remain unclear. In this study, we investigated the expression of EDA2R in balding HFs and matched with non-balding HFs. The EDA2R level was upregulated in the balding dermal papilla (DP) cells compared with non-balding DP cells derived from patients with AGA. However, EDA2R was strongly expressed in both balding and non-balding outer root sheath (ORS) cells. We screened EDA-A2-regulated genes in balding DP cells and identified dickkopf 1 (DKK-1) as catagen inducer during the hair cycle. The mRNA and protein expression levels of DKK-1 were both upregulated by EDA-A2. In addition, DKK-1 expression was induced by EDA-A2 both in cultured human HFs and in mouse HFs. Moreover, the EDA-A2-induced apoptosis of DP and ORS cells was reversed by the antibody-mediated neutralization of DKK-1. Collectively, our data strongly suggest that EDA-A2 induces DKK-1 secretion and causes apoptosis in HFs by binding EDA2R, which is overexpressed in the bald scalp. EDA-A2/EDA2R signaling could inhibit hair growth through DKK-1 induction, and an inhibitor of EDA-A2/EDA2R signaling may be a promising agent for the treatment and prevention of AGA.
Mi Hee Kwack, Mee Sook Jun, Young Kwan Sung, Jung Chul Kim, Moon Kyu Kim

1096 related Products with: Ectodysplasin-A2 induces dickkopf 1 expression in human balding dermal papilla cells overexpressing the ectodysplasin A2 receptor.

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#32714315   2020/07/02 To Up

Influence of Androgens on Immunity to Self and Foreign: Effects on Immunity and Cancer.

It is well-known that sex hormones can directly and indirectly influence immune cell function. Different studies support a suppressive role of androgens on different components of the immune system by decreasing antibody production, T cell proliferation, NK cytotoxicity, and stimulating the production of anti-inflammatory cytokines. Androgen receptors have also been detected in many different cells of hematopoietic origin leading to direct effects of their ligands on the development and function of the immune system. The immunosuppressive properties of androgens could contribute to gender dimorphisms in autoimmune and infectious disease and thereby also hamper immune surveillance of tumors. Consistently, females generally are more prone to autoimmunity, while relatively less susceptible to infections, and have lower incidence and mortality of the majority of cancers compared to males. Some studies show that androgen deprivation therapy (ADT) can induce expansion of naïve T cells and increase T-cell responses. Emerging clinical data also reveal that ADT might enhance the efficacy of various immunotherapies including immune checkpoint blockade. In this review, we will discuss the potential role of androgens and their receptors in the immune responses in the context of different diseases. A particular focus will be on cancer, highlighting the effect of androgens on immune surveillance, tumor biology and on the efficacy of anti-cancer therapies including emerging immune therapies.
Isabel Ben-Batalla, María Elena Vargas-Delgado, Gunhild von Amsberg, Melanie Janning, Sonja Loges

1464 related Products with: Influence of Androgens on Immunity to Self and Foreign: Effects on Immunity and Cancer.

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#32685034   // To Up

INSIGHTS ON AROMATASE IMMUNOHISTOCHEMISTRY: VARIATIONS BETWEEN INTRINSIC MOLECULAR SUBTYPES OF BREAST CANCERS.

Aromatase is a key enzyme in local estrogen production by androgen conversion, especially in women post-menopause. There have been controversies concerning aromatase localization in breast carcinomas and its association with current histopathological variables.
I Armasu, C Preda, V Ianole, V Mocanu, I Hristov, E C Andriescu, I Cretu-Silivestru, I Vasiliu, C G Dascalu, C D Lupascu, I Crumpei, D N Serban, I L Serban, D G Ciobanu Apostol

1016 related Products with: INSIGHTS ON AROMATASE IMMUNOHISTOCHEMISTRY: VARIATIONS BETWEEN INTRINSIC MOLECULAR SUBTYPES OF BREAST CANCERS.

2x5L100ul 6 ml 6 ml Ready-to-use

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#32619831   2020/06/23 To Up

Antibody selection influences the detection of AR-V7 in primary prostate cancer.

The androgen receptor (AR) splice variant V7 (AR-V7) is an emerging marker to aid clinical decision-making in patients with castration-resistant prostate cancer (CRPC). A number of studies have shown that a subset of patients also express AR-V7 in the primary tumor. These findings have recently been challenged by a study showing that AR-V7 becomes only detectable in CRPC but is virtually absent in castration-naïve prostate cancer.
Adam Kaczorowski, Xin Chen, Esther Herpel, Axel S Merseburger, Glen Kristiansen, Christof Bernemann, Markus Hohenfellner, Marcus V Cronauer, Stefan Duensing

1463 related Products with: Antibody selection influences the detection of AR-V7 in primary prostate cancer.

100ug

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#32602285   // To Up

NANOG as prognostic factor of prostate cancer course.

The variability of the clinical course of prostate cancer (PC) indicates the need to find factors that could predict the aggressive potential of neoplasms accounting the biological characteristics of tumor cells. In this context, the role of NANOG, a transcription factor involved in maintaining pluripotency and one of the markers of cancer stem cells (CSCs), is being actively studied today.
T V Zadvornyi, N Yu Lukianova, T V Borikun, Yu V Vitruk, E O Stakhovsky, V F Chekhun

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#32568835   2020/06/15 To Up

Twenty-Eight Cases of Extraocular Sebaceous Carcinoma: A Correlative Clinicopathological and Immunohistochemical Analysis of Extraocular Sebaceous Carcinomas and Benign Sebaceous Gland Tumors.

Extraocular sebaceous carcinoma (ESC) is a rare appendiceal skin tumor. In contrast to ocular sebaceous carcinoma, information about the exact cellular architecture of these lesions is scarce and the histogenesis of ESC is unknown. Here, we extend our previous study and investigate 28 extraocular carcinomas in comparison to 54 benign sebaceous tumors and 8 cases of normal sebaceous glands using a broad spectrum of antibodies against p63, several keratins, adipophilin, EMA, Ki67, androgen receptor, and mismatch repair proteins. This observational study demonstrates that p63- and K5/14-positive basaloid cells are key cells in normal sebaceous gland and in all sebaceous tumors and that these basaloid cells give rise to EMA+, adipophilin+ sebocytes, and K5/14+, K7±, K10± ductal structures. Finally, about half of ESC is associated with superficial in situ neoplasia, which provides evidence that at least part of these carcinomas arises from flat superficial in situ carcinoma. In contrast to the normal sebaceous gland, about half of all sebaceous tumors lack keratin K7. MMR protein IHC-profiles role will be discussed.
Werner Boecker, Michael Reusch, Volker Mielke, Ursula Reusch, Christian Hallermann, Thomas Loening, Markus Tiemann, Igor Buchwalow

1873 related Products with: Twenty-Eight Cases of Extraocular Sebaceous Carcinoma: A Correlative Clinicopathological and Immunohistochemical Analysis of Extraocular Sebaceous Carcinomas and Benign Sebaceous Gland Tumors.

10 mg

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#32560654   2020/06/19 To Up

Early upregulation of AR and steroidogenesis enzyme expression after 3 months of androgen-deprivation therapy.

Androgen deprivation therapy (ADT) is a standard treatment for advanced prostate cancer (PCa). However, PCa recurrence and progression rates during ADT are high. Until now, there has been no evidence regarding when progression begins. This study evaluated the gene expression of intraprostatic androgen receptor (AR) and steroidogenic enzymes in the early stages of ADT.
Agus Rizal A H Hamid, Harun W Kusuma Putra, Ningrum Paramita Sari, Putri Diana, Saras Serani Sesari, Eka Novita, Fajar Lamhot Gultom, Meilania Saraswati, Budiana Tanurahardja, Asmarinah, Rainy Umbas, Chaidir A Mochtar

2965 related Products with: Early upregulation of AR and steroidogenesis enzyme expression after 3 months of androgen-deprivation therapy.

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#32532924   2020/06/12 To Up

Genetic signature of prostate cancer mouse models resistant to optimized hK2 targeted α-particle therapy.

Hu11B6 is a monoclonal antibody that internalizes in cells expressing androgen receptor (AR)-regulated prostate-specific enzyme human kallikrein-related peptidase 2 (hK2; ). In multiple rodent models, Actinium-225-labeled hu11B6-IgG ([Ac]hu11B6-IgG) has shown promising treatment efficacy. In the present study, we investigated options to enhance and optimize [Ac]hu11B6 treatment. First, we evaluated the possibility of exploiting IgG, the IgG subclass with superior activation of complement and ability to mediate FC-γ-receptor binding, for immunotherapeutically enhanced hK2 targeted α-radioimmunotherapy. Second, we compared the therapeutic efficacy of a single high activity vs. fractionated activity. Finally, we used RNA sequencing to analyze the genomic signatures of prostate cancer that progressed after targeted α-therapy. [Ac]hu11B6-IgG was a functionally enhanced alternative to [Ac]hu11B6-IgG but offered no improvement of therapeutic efficacy. Progression-free survival was slightly increased with a single high activity compared to fractionated activity. Tumor-free animals succumbing after treatment revealed no evidence of treatment-associated toxicity. In addition to up-regulation of canonical aggressive prostate cancer genes, such as , , , and , we also noted a significant decrease in both (prostate-specific antigen ) and (prostate-specific membrane antigen) but not in and , demonstrating efficacy of sequential [Ac]hu11B6 in a mouse model.
Mesude Bicak, Katharina Lückerath, Teja Kalidindi, Michael E Phelps, Sven-Erik Strand, Michael J Morris, Caius G Radu, Robert Damoiseaux, Mari T Peltola, Norbert Peekhaus, Austin Ho, Darren Veach, Ann-Christin Malmborg Hager, Steven M Larson, Hans Lilja, Michael R McDevitt, Robert J Klein, David Ulmert

1762 related Products with: Genetic signature of prostate cancer mouse models resistant to optimized hK2 targeted α-particle therapy.

1 kit(96 Wells)100 ug1.00 ml100 ug100 1 kitOne 96-Well Strip Micropl100

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#32473708   2020/01/23 To Up

Macrophages affect immune inflammation and proliferation in benign prostatic hyperplasia via androgen receptor and CD40/CD40L signaling pathway.

Considering the association of macrophage migration inhibitory factor with development of prostate diseases, this study aims to explore the effect and mechanism of macrophages (MAs) in inflammation and proliferation of benign prostate hyperplasia (BPH) cells.
Minggen Yang, Zhenqiang Xu, Zhiming Zhuang

1038 related Products with: Macrophages affect immune inflammation and proliferation in benign prostatic hyperplasia via androgen receptor and CD40/CD40L signaling pathway.

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