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Special Issue "Hormone Receptors in Genitourinary Tumors"

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A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (31 May 2018) | Viewed by 24409

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Special Issue Editor

Prof. Hiroshi Miyamoto

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Guest Editor

Director of Genitourinary Pathology, University of Rochester Medical Center, Rochester, NY, USA
Interests: nuclear hormone receptors; androgen receptor; glucocorticoid receptor; antiandrogens; glucocorticoids; urothelial cancer; prostate cancer; genitourinary pathology
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Special Issue Information

Dear Colleagues,

Hormone receptors that bind to specific hormones are known to have widespread physiological functions. Recently, a large body of evidence has emerged suggesting that hormone receptors play a role in the development and progression of various types of malignancies, although their exact functions are not fully characterized. The aim of this Special Issue is to provide an overview of current preclinical and clinical findings indicating the involvement of hormone receptor signals in genitourinary tumors including prostate cancer, as well as renal cancer, upper urinary tract cancer, bladder cancer, and testicular cancer that have not traditionally been considered as endocrine neoplasms. Original research or review articles on signaling related to any hormone receptors in urological tumors would be most welcome.

Prof. Dr. Hiroshi Miyamoto
Guest Editor

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Keywords

androgen receptor
estrogen receptor
glucagon receptor
glucocorticoid receptor
gonadotropin receptors
luteinizing receptor
progesterone receptor
orphan receptor
retinoid receptor
somatostatin receptor
vitamin D receptor
prostate cancer
renal cancer
testicular cancer
urothelial cancer

Published Papers (4 papers)

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Review

Open AccessReview

The Role of Glucocorticoid Receptor Signaling in Bladder Cancer Progression

Hiroki Ide

Satoshi Inoue

and

Hiroshi Miyamoto

Cancers 2018, 10(12), 484; https://doi.org/10.3390/cancers10120484 - 04 Dec 2018

Cited by 11 | Viewed by 2868

Abstract

Previous preclinical studies have indicated that the activation of glucocorticoid receptor signaling results in inhibition of the growth of various types of tumors. Indeed, several glucocorticoids, such as dexamethasone and prednisone, have been prescribed for the treatment of, for example, hematological malignancies and castration-resistant prostate cancer. By contrast, the role of glucocorticoid-mediated glucocorticoid receptor signaling in the progression of bladder cancer remains far from being fully understood. Nonetheless, emerging evidence implies its unique functions in urothelial cancer cells. Moreover, the levels of glucocorticoid receptor expression have been documented to significantly associate with the prognosis of patients with bladder cancer. This review summarizes the available data suggesting the involvement of glucocorticoid-mediated glucocorticoid receptor signaling in urothelial tumor outgrowth and highlights the potential underlying molecular mechanisms. The molecules/pathways that contribute to modulating glucocorticoid receptor activity and function in bladder cancer cells are also discussed. Full article

(This article belongs to the Special Issue Hormone Receptors in Genitourinary Tumors)

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Open AccessEditor’s ChoiceReview

Targeting Crosstalk between Nrf-2, NF-κB and Androgen Receptor Signaling in Prostate Cancer

Namrata Khurana

and

Suresh C. Sikka

Cancers 2018, 10(10), 352; https://doi.org/10.3390/cancers10100352 - 25 Sep 2018

Cited by 61 | Viewed by 6797

Abstract

Oxidative stress, inflammation and androgen receptor (AR) signaling play a pivotal role in the initiation, development and progression of prostate cancer (PCa). Numerous papers in the literature have documented the interconnection between oxidative stress and inflammation; and how antioxidants can combat the inflammation. It has been shown in the literature that both oxidative stress and inflammation regulate AR, the key receptor involved in the transition of PCa to castration resistant prostate cancer (CRPC). In this review, we discuss about the importance of targeting Nrf-2-antioxidant signaling, NF-κB inflammatory response and AR signaling in PCa. Finally, we discuss about the crosstalk between these three critical pathways as well as how the anti-inflammatory antioxidant phytochemicals like sulforaphane (SFN) and curcumin (CUR), which can also target AR, can be ideal candidates in the chemoprevention of PCa. Full article

(This article belongs to the Special Issue Hormone Receptors in Genitourinary Tumors)

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Open AccessReview

Castration-Resistant Prostate Cancer Refractory to Second-Generation Androgen Receptor Axis-Targeted Agents: Opportunities and Challenges

and

Cancers 2018, 10(10), 345; https://doi.org/10.3390/cancers10100345 - 21 Sep 2018

Cited by 19 | Viewed by 5253

Abstract

Second-generation androgen receptor axis-targeted (ARAT) agents, namely abiraterone and enzalutamide, enable stronger blockade of the androgen receptor (AR) axis and longer survival of men with castration-resistant prostate cancer (CRPC). However, the extent of the improved survival remains insufficient and the majority of patients eventually develop resistance to these novel agents. Some patients develop resistance against ARAT treatment through mechanisms termed “complete AR independence” or “AR indifference”, and no longer require activation of the AR axis. However, a considerable proportion of CRPC patients remain persistently dependent on AR or its downstream signaling pathways. Ligand-independent activation of the AR, an AR axis-dependent mechanism, is mediated by truncated forms of ARs that lack the ligand-binding domain (LBD), arising as products of AR splicing variants or nonsense mutations of AR. Post-translational modifications of ARs can also contribute to ligand-independent transactivation of the AR. Other mechanisms for AR axis activation are mediated by pathways that bypass the AR. Recent studies revealed that the glucocorticoid receptor can upregulate a similar transcription program to that of the AR, thus bypassing the AR. ARAT agents are essentially ineffective for CRPC driven by these AR-independent mechanisms. This review article describes recent efforts to overcome these refractory machineries for the development of next-generation AR axis blockade in CRPC. Full article

(This article belongs to the Special Issue Hormone Receptors in Genitourinary Tumors)

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Open AccessEditor’s ChoiceReview

Estrogen and Androgen Blockade for Advanced Prostate Cancer in the Era of Precision Medicine

and

Cancers 2018, 10(2), 29; https://doi.org/10.3390/cancers10020029 - 23 Jan 2018

Cited by 24 | Viewed by 8813

Abstract

Androgen deprivation therapy (ADT) has been widely prescribed for patients with advanced prostate cancer (PC) to control key signaling pathways via androgen receptor (AR) and AR-collaborative transcriptional factors; however, PC gradually acquires a lethal phenotype and results in castration-resistant PC (CRPC) during ADT. Therefore, new therapeutic strategies are required in clinical practice. In addition, ARs; estrogen receptors (ERs; ERα and ERβ); and estrogen-related receptors (ERRs; ERRα, ERRβ, and ERRγ) have been reported to be involved in the development or regulation of PC. Recent investigations have revealed the role of associated molecules, such as KLF5, FOXO1, PDGFA, VEGF-A, WNT5A, TGFβ1, and micro-RNA 135a of PC, via ERs and ERRs. Selective ER modulators (SERMs) have been developed. Recently, estrogen and androgen blockade (EAB) using a combination of toremifene and ADT has been demonstrated to improve biochemical recurrence rate in treatment-naïve bone metastatic PC. In the future, the suitability of ADT alone or EAB for individuals may be evaluated by making clinical decisions on the basis of information obtained from RT-PCR, gene-panel, or liquid biopsy to create a “personalized medicine” or “precision medicine”. In this review, we summarize ER and ERR signaling pathways, molecular diagnosis, and SERMs as candidates for advanced PC treatment. Full article

(This article belongs to the Special Issue Hormone Receptors in Genitourinary Tumors)

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Special Issue "Hormone Receptors in Genitourinary Tumors"

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