Immunohistochemistry of the Androgen Receptor in Human Benign and Malignant Prostate Tissue

Miyamoto, Kent K.; McSherry, Susan A.; Dent, Georgette A.; Sar, Madhabananda; Wilson, Elizabeth M.; French, Frank S.; Sharief, Yousuf; Mohler, James L.

doi:10.1016/s0022-5347(17)36284-5

Cited by 68 publications

(35 citation statements)

References 18 publications

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“…[34][35][36][37] Recent work has focused on AR overexpression in hormonerefractory PCa where immunostaining for AR was more intense in tumors with amplification of the AR gene. 38 However, our patient cohort consisted entirely of hormone-sensitive PCas, for which AR amplification is not likely a contributory mechanism.…”

Section: Discussionmentioning

confidence: 99%

Androgen receptor CAG repeat length contraction in diseased and non-diseased prostatic tissues

Sircar

Gottlieb

Alvarado

et al. 2007

Prostate Cancer Prostatic Dis

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Section: Discussionmentioning

confidence: 99%

Androgen receptor CAG repeat length contraction in diseased and non-diseased prostatic tissues

Sircar

Gottlieb

Alvarado

et al. 2007

Prostate Cancer Prostatic Dis

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“…The percentage (0-100%) of nuclei staining at each staining intensity level was determined. A nuclear scoring system was subsequently done as described previously (27). Nuclear score (ranging 0-300) was calculated by a formula as follows: 0 Â a% + 1 Â b% + 2 Â c% + 3 Â d%, in which a, b, c, and d were percentages of nuclei stained at different staining intensity grades.…”

Section: Translational Relevancementioning

confidence: 99%

Suppression of Androgen-Independent Prostate Cancer Cell Aggressiveness by FTY720: Validating Runx2 as a Potential Antimetastatic Drug Screening Platform

Chua¹,

Chiu²,

Yuen³

et al. 2009

Clinical Cancer Research

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Purpose: Previously, FTY720 was found to possess potent anticancer effects on various types of cancer. In the present study, we aimed to first verify the role of Runx2 in prostate cancer progression and metastasis, and, subsequently, assessed if FTY720 could modulate Runx2 expression, thus interfering downstream events regulated by this protein.Experimental Design: First, the association between Runx2 and prostate cancer progression was assessed using localized prostate cancer specimens and mechanistic investigation of Runx2-induced cancer aggressiveness was then carried out. Subsequently, the effect of FTY720 on Runx2 expression and transcriptional activity was investigated using PC-3 cells, which highly expressed Runx2 protein. Last, the involvement of Runx2 in FTY720-induced anticancer effects was evaluated by modulating Runx2 expression in various prostate cancer cell lines. Results: Runx2 nuclear expression was found to be up-regulated in prostate cancer and its expression could be used as a predictor of metastasis in prostate cancer. Further mechanistic studies indicated that Runx2 accelerated prostate cancer aggressiveness through promotion of cadherin switching, invasion toward collagen I, and Akt activation. Subsequently, we found that FTY720 treatment down-regulated Runx2 expression and its transcriptional activity, as well as inhibited its regulated downstream events. More importantly, silencing Runx2 in PC-3 enhanced FTY720-induced anticancer effects as well as cell viability inhibition, whereas overexpressing Runx2 in 22Rv1that expressed very low endogenous Runx2 protein conferred resistance in the same events. Conclusion: This study provided a novel mechanism for the anticancer effect of FTY720 on advanced prostate cancer, thus highlighting the therapeutic potential of this drug in treating this disease.

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“…[19] Tissue preservation of immunoreactivity was enhanced by mounting tissue onto rat-liver homogenate as an adhesive and rapid freezing in isopentane cooled by liquid nitrogen. AR immunostaining was characterized by both intensity of, and variation in, intensity of immunostaining using a visual scoring index.…”

Section: Androgen-receptor Expression In the Epithelia Of Clinically mentioning

confidence: 99%

“…The first study of AR protein expression in prostate tissue used frozen sections, visual scoring, and a polyclonal antibody. [19] The discovery of methods for antigen retrieval from archived clinical specimens [61] and the development of a highly specific monoclonal antibody allowed correlation between AR protein expression and clinical parameters of interest. Antigen retrieval is best performed using Reveal Citra buffer (Biocare Medical, Walnut Creek, CA, USA) and a pressurized antigen-decloaking chamber for 2 minutes at 120°C and 21 PSI.…”

Section: Accurate Measurement Of Androgen-receptor Expression In Clinmentioning

confidence: 99%

A role for the androgen-receptor in clinically localized and advanced prostate cancer

Mohler

2008

Best Practice & Research Clinical Endocrinology & Metab

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Earlier studies of androgen-receptor (AR) expression using frozen prostate tissue, and later studies using archived specimens, produced the consensus that ligand-stabilized AR is nuclear, AR expression is similar in benign epithelia and stroma, AR expression is greater in secretory epithelia than basal cells, and AR expression is more variable in prostate cancer (CaP) than in benign prostatic hyperplasia (BPH). Accurate measurement of AR expression remains technically challenging but necessary to evaluate the relevance of ARs to clinical CaP. Recent studies demonstrated that AR expression in epithelia and stroma may be prognostic in clinically localized CaP, and AR expression may play a role in racial differences in CaP mortality and predict response to androgen deprivation therapy. High levels of AR and AR-regulated gene expression indicate a central role for AR in growth regulation of castration-recurrent CaP. New treatments for the lethal phenotype of CaP require better understanding of AR transactivation during androgen deprivation therapy. Keywordsandrogen receptor; prostate cancer; quantitative video image analysis; immunohistochemistry Androgens are necessary for the development and growth of the prostate and for the development, growth and progression of prostate cancer (CaP). An American man is diagnosed with CaP every 3 minutes,[1] and the worldwide incidence of CaP is increasing an estimated 1.1% annually.[2] Despite increased use of digital rectal examination and serum prostatespecific antigen (PSA) measurement for early detection, approximately 30% of men treated with curative intent suffer CaP recurrence. These men, and those who present with locally advanced or metastatic CaP, can be palliated by androgen deprivation therapy (ADT), which causes regression of androgen-dependent CaP through programmed cell death.[3] Although there are many methods for medical and surgical ADT, the results of ADT remain unimproved since its discovery more than 60 years ago.[4] More than 80% of men with disseminated CaP demonstrate clinical or biochemical response that is associated with a mean life expectancy of approximately 3.5 years, in contrast to non-responders or untreated patients who live an average of 9 months. Regardless of the androgen responsiveness of incurable CaP, almost all patients succumb to castration-recurrent CaP because it responds poorly to all known therapies, and

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Immunohistochemistry of the Androgen Receptor in Human Benign and Malignant Prostate Tissue

Cited by 68 publications

References 18 publications

Androgen receptor CAG repeat length contraction in diseased and non-diseased prostatic tissues

Androgen receptor CAG repeat length contraction in diseased and non-diseased prostatic tissues

Suppression of Androgen-Independent Prostate Cancer Cell Aggressiveness by FTY720: Validating Runx2 as a Potential Antimetastatic Drug Screening Platform

A role for the androgen-receptor in clinically localized and advanced prostate cancer

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