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Search results for: Androgen Receptor Ab 1

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#34337539   2021/06/12 To Up

Decreased ATM Protein Expression Is Substantiated with PTEN Loss in Defining Aggressive Phenotype of Prostate Cancer Associated with Lethal Disease.

Ataxia Telangiectasia Mutated (ATM) serine/threonine protein kinase is a known tumor suppressor, involved in DNA damage repair. It has prognostic and predictive therapeutic implications and is associated with aggressive prostate cancer (PCa).
Simon R Walker, Ramy Abdelsalam, Sunita Ghosh, Julie Livingstone, Nallasivam Palanisamy, Paul C Boutros, Steven M Yip, Susan P Lees-Miller, Tarek A Bismar

2926 related Products with: Decreased ATM Protein Expression Is Substantiated with PTEN Loss in Defining Aggressive Phenotype of Prostate Cancer Associated with Lethal Disease.

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#34175318   2021/06/25 To Up

Uterine anomalies in cell proliferation, energy homeostasis and oxidative stress in PCOS hamsters, M. auratus: Therapeutic potentials of melatonin.

Polycystic ovarian syndrome (PCOS) is a reproductive, endocrine and metabolic disorder. Less is known about the mechanism of its effect on uterine function and therapeutic potential of melatonin. Our aim was to evaluate uterine dysfunction(s) in letrozole induced PCOS and its possible rectification by melatonin.
Shruti R Hansda, Chandana Haldar

2155 related Products with: Uterine anomalies in cell proliferation, energy homeostasis and oxidative stress in PCOS hamsters, M. auratus: Therapeutic potentials of melatonin.

100 ml.25 ml.96 tests100ug Lyophilized1 mL100ug Lyophilized24 tests

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#34161185   2021/06/23 To Up

Autophagy in ovary and polycystic ovary syndrome: role, dispute and future perspective.

Polycystic ovary syndrome (PCOS) is a unification of endocrine and metabolic disorders and has become immensely prevalent among women of fertile age. The prime organ affected in PCOS is the ovary and its distressed functioning elicits disturbed reproductive outcomes. In the ovary, macroautophagy/autophagy performs a pivotal role in directing the chain of events starting from oocytes origin until its fertilization. Recent discoveries demonstrate a significant role of autophagy in the pathogenesis of PCOS. Defective autophagy in the follicular cells during different stages of follicles is observed in the PCOS ovary. Exploring different autophagy pathways provides a platform for predicting the possible cause of altered ovarian physiology in PCOS. In this review, we have emphasized autophagy's role in governing follicular development under normal circumstances and in PCOS, including significant abnormalities associated with PCOS such as anovulation, hyperandrogenemia, metabolic disturbances, and related abnormality. So far, few studies have linked autophagy and PCOS and propose its essential role in PCOS progression. However, detailed knowledge in this area is lacking. Here we have summarized the latest knowledge related to autophagy associated with PCOS. This review's main objective is to provide a background of autophagy in the ovary, its possible connection with PCOS and suggested a novel proposal for future studies to aid a better understanding of PCOS pathogenesis.: AE: androgen excess; AF: antral follicle; AKT/PKB: AKT serine/threonine kinase; AMH: anti-Mullerian hormone; AMPK: AMP-activated protein kinase; ATG: autophagy-related; BCL2: BCL2 apoptosis regulator; BECN1: beclin 1; BMP: bone morphogenetic protein; CASP3: caspase 3; CL: corpus luteum; CYP17A1/P450C17: cytochrome P450 family 17 subfamily A member 1; CYP19A1: cytochrome P450 family 19 subfamily A member 1; DHEA: dehydroepiandrosterone; EH: endometrial hyperplasia; FF: follicular fluid; FOXO: forkhead box O; FSH: follicle stimulating hormone; GC: granulosa cell; GDF: growth differentiation factor; HA: hyperandrogenemia; HMGB1: high mobility group box 1; IGF1: insulin like growth factor 1; INS: insulin; IR: insulin resistance; LHCGR/LHR: luteinizing hormone/choriogonadotropin receptor; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MAPK/ERK: mitogen-activated protein kinase; MAPK8/JNK: mitogen-activated protein kinase 8; MTOR: mechanistic target of rapamycin kinase; MTORC: mechanistic target of rapamycin complex; NAFLD: nonalcoholic fatty liver disease; NFKB: nuclear factor kappa B; OLR1/LOX-1: oxidized low density lipoprotein receptor 1; oxLDL: oxidized low-density lipoproteins; PA: palmitic acid; PCOS: polycystic ovary syndrome; PF: primary follicle; PGC: primordial germ cell; PI3K: phosphoinositide 3-kinase; PMF: primordial follicle; ROS: reactive oxygen species; RP: resting pool; SIRT1: sirtuin 1; SQSTM1/p62: sequestosome 1; T2DM: type 2 diabetes mellitus; TC: theca cell; TUG1: taurine up-regulated 1.
Sanjana Kumariya, Vaibhave Ubba, Rajesh K Jha, Jiaur R Gayen

1019 related Products with: Autophagy in ovary and polycystic ovary syndrome: role, dispute and future perspective.



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#34119408   2021/06/09 To Up

Nonclassical androgen and estrogen signaling is essential for normal spermatogenesis.

Signaling by androgens through androgen receptor (AR) is essential to complete spermatogenesis in the testis. Similarly, loss of the main estrogen receptor, estrogen receptor 1 (ESR1; also known as ERα), results in male infertility, due in part to indirect deleterious effects on the seminiferous epithelium and spermatogenesis. Effects of steroid hormones are induced primarily through genomic changes induced by hormone-mediated activation of their intracellular receptors and subsequent effects on nuclear gene transcription. However, androgens and estrogens also signal through rapid nonclassical pathways involving actions initiated at the cell membrane. Here we review the data that nonclassical androgen and estrogen signaling pathways support processes essential for male fertility in the testis and reproductive tract. The recent development of transgenic mice lacking nonclassical AR or ESR1 signaling but retaining genomic nuclear signaling has provided a powerful tool to elucidate the function of nonclassical signaling in the overall response to androgens and estrogens. Results from these mice have emphasized that nonclassical signaling is essential for full responses to these hormones, and absence of either nonclassical or classical AR or ESR1 pathways produces abnormalities in spermatogenesis and the male reproductive tract. Although additional work is required to fully understand how classical and nonclassical receptor signaling synergize to produce full steroid hormone responses, here we summarize the known physiological functions of the classical and nonclassical androgen and estrogen signaling pathways in the testis and reproductive tract.
Paul S Cooke, William H Walker

2481 related Products with: Nonclassical androgen and estrogen signaling is essential for normal spermatogenesis.

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#34032505   2021/05/25 To Up

Cardiovascular Proteomics: A Post Hoc Analysis from a Phase II Randomized Clinical Trial Comparing GnRH Antagonist vs GnRH Agonist among Men with Advanced Prostate Cancer.

Recent studies demonstrated reduced cardiovascular (CV) risk with gonadotropin-releasing hormone (GnRH) antagonist, yet the underlying mechanism remains undetermined. The objective of this study was to examine longitudinal changes over time in established CV related proteins among men treated with GnRH agonists vs GnRH antagonist.
Karin Lifshitz, Yaara Ber, Chen Shenhar, Jan Nillson, Avivit Peer, Eli Rosenbaum, Jack Baniel, Daniel Kedar, Osnat Itzhaki Ben Zadok, David Margel

2301 related Products with: Cardiovascular Proteomics: A Post Hoc Analysis from a Phase II Randomized Clinical Trial Comparing GnRH Antagonist vs GnRH Agonist among Men with Advanced Prostate Cancer.



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#33794293   2021/03/29 To Up

Plasma tumor gene conversions after one cycle abiraterone acetate for metastatic castration-resistant prostate cancer: a biomarker analysis of a multicenter international trial.

Plasma tumor DNA fraction is prognostic in metastatic cancers. This could improve risk stratification before commencing a new treatment. We hypothesized that a second sample collected after one cycle of treatment could refine outcome prediction of patients identified as poor prognosis based on plasma DNA collected pre-treatment.
A Jayaram, A Wingate, D Wetterskog, G Wheeler, C N Sternberg, R Jones, A Berruti, F Lefresne, M Lahaye, S Thomas, M Gormley, F Meacham, K Garg, L P Lim, A S Merseburger, B Tombal, D Ricci, G Attard

2982 related Products with: Plasma tumor gene conversions after one cycle abiraterone acetate for metastatic castration-resistant prostate cancer: a biomarker analysis of a multicenter international trial.



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#33723169   // To Up

Complete androgen insensitivity syndrome with intra-abdominal seminoma in a phenotypic female: A rare presentation.

Androgen insensitivity syndrome (AIS) is a rare, X-linked recessive disorder which causes alterations in androgen receptor gene leading to hormone resistance, which may present clinically under three phenotypes: complete AIS (CAIS), partial AIS, or mild AIS. The symptoms range from phenotypically normal males with impaired spermatogenesis to phenotypically normal women with primary amenorrhea. We report a case of a 35-year-old woman who was diagnosed with CAIS and presented with malignant transformation of the undescended testis. The histopathology confirmed the presence of seminoma. In this case report, we reviewed the literature which describes the biochemical and endocrinological abnormalities leading to the syndrome. It also highlights the potential for malignant changes of the undescended testes, diagnosis, and therapeutic management.
Savita Arora, Neha Sharma, Arun Kumar Rathi, Kishore Singh, Kavita Sehrawat

1115 related Products with: Complete androgen insensitivity syndrome with intra-abdominal seminoma in a phenotypic female: A rare presentation.

100 μg100ug Lyophilized100 μg1 Set100 assays1 Set

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#33548512   2021/02/04 To Up

GREB1L as a candidate gene of Mayer-Rokitansky-Küster-Hauser Syndrome.

Mayer-Rokitansky-Küster-Hauser (MRKH) Syndrome is a sex development disorder that affects 1 in every 4500 46, XX live births. At least a subset of MRKH syndrome is genetically related to which various candidate genes have been identified. The growth regulation by estrogen in breast cancer 1-like gene (GREB1L) is an androgen-regulated gene reported to be a co-activator of the retinoic acid receptor gene (RAR). Thus expression levels of GREB1L have implications on renal system cellular differentiation, morphogenesis, and homeostasis in vertebrates. Variants of GREB1L have been reported in familial and sporadic MRKH Syndrome and more importantly, in a three-generation family ofMRKH syndrome propositae. Much the same way, Mutants of GREB1L have also been identified in isolated bilateral renal agenesis and deafness both of which are extra-genital tract anomalies in MRKH type 2. Again, renal agenesis transgenic mice have been produced from an E13.5 CRISPR/cas9 GREB1L mutagenesis. Though no GREB1L mutation has been reported in cardiac malformation, there is evidence that GREB1L is involved in ventricular development. Here, we intorigate evidence that projects GREB1L as a candidate gene of Mayer-Rokitansky-Küster-Hauser Syndrome and propose that functional validation analysis to that effect is imparative.
Isaac Kyei Barffour, Roselind Kyei Baah Kwarkoh

2879 related Products with: GREB1L as a candidate gene of Mayer-Rokitansky-Küster-Hauser Syndrome.

10 plates1 kit1 plate2001 plate96 assays 1000100 plates

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#33522043   2021/02/09 To Up

Landscape of Cyclin Pathway Genomic Alterations Across 5,356 Prostate Cancers: Implications for Targeted Therapeutics.

The cyclin pathway may confer resistance to standard treatments but also offer novel therapeutic opportunities in prostate cancer. Herein, we analyzed prostate cancer samples (majority metastatic) using comprehensive genomic profiling performed by next-generation sequencing (315 genes, >500× coverage) for alterations in activating and sensitizing cyclin genes (CDK4 amplification, CDK6 amplification, CCND1, CCND2, CCND3, CDKN2B [loss], CDKN2A [loss], SMARCB1), androgen receptor (AR) gene, and coalterations in genes leading to cyclin inhibitor therapeutic resistance (RB1 and CCNE1). Overall, cyclin sensitizing pathway genomic abnormalities were found in 9.7% of the 5,356 tumors. Frequent alterations included CCND1 amplification (4.2%) and CDKN2A and B loss (2.4% each). Alterations in possible resistance genes, RB1 and CCNE1, were detected in 9.7% (up to 54.6% in neuroendocrine) and 1.2% of cases, respectively, whereas AR alterations were seen in 20.9% of tumors (~27.3% in anaplastic). Cyclin sensitizing alterations were also more frequently associated with concomitant AR alterations.
Denis L Jardim, Sherri Z Millis, Jeffrey S Ross, Michelle Sue-Ann Woo, Siraj M Ali, Razelle Kurzrock

1477 related Products with: Landscape of Cyclin Pathway Genomic Alterations Across 5,356 Prostate Cancers: Implications for Targeted Therapeutics.

1 G 5 G2 Pieces/Box0.1 mg10, 10ml whole blood 1 G1.0 mg100 TESTS2 Pieces/Box100μg

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