Special Issue "Sex Hormone Receptor Signals in Human Malignancies"
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: 30 November 2018
Dr. Hiroshi Miyamoto
Departments of Pathology & Laboratory Medicine, Oncology, and Urology, University of Rochester Medical Center, Rochester, NY, USA
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Interests: nuclear hormone receptors; androgen receptor; glucocorticoid receptor; antiandrogens; glucocorticoids; urothelial cancer; prostate cancer; genitourinary pathology
Sex steroids, including androgens, estrogens, and progestogens, are known to have widespread physiological actions beyond the reproductive system via binding to the sex hormone receptors, members of the nuclear receptor superfamily that function as ligand-inducible transcription factors. Meanwhile, the roles of androgen receptor and estrogen/progesterone receptors have been widely studied in prostate and breast cancers, respectively. However, emerging evidence implies that sex hormone receptor signals play a role in the development and progression of various other types of malignancies, although their exact functions are not fully characterized. These malignancies include, but are not limited to, endometrial cancer, ovarian cancer, urothelial tumor of the bladder or upper urinary tract, liver cancer, lung cancer, and gastrointestinal cancer. Thus, the aim of this Special Issue is to provide an overview of current preclinical and clinical findings indicating the involvement of sex hormone receptor signals in human malignancies that have not traditionally been considered as endocrine neoplasms. Original research or review articles on androgen/estrogen/progesterone receptor signaling in prostate or breast cancer would also be most welcome.
Dr. Hiroshi Miyamoto
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- androgen receptor
- estrogen receptor
- progesterone receptor
- prostate cancer
- breast cancer
- female reproductive system cancer
- urothelial cancer
- liver cancer
- lung cancer
- gastrointestinal cancer
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: Small Molecule Targeting of the Glucocorticoid Receptor Suppresses the AR-V7 Transcriptome
Authors: David Mulholland, Lin Wang, Geoffrey Bryant, Guilhem Roubaud
Abstract: Enzalutamide resistance is postulated to correspond with elevated expression and activity of the Glucocorticoid Receptor Signaling Axis. However, the manner in which compensatory GR function facilitates continued survival in prostate cancer cells remains unclear. Using newly developed small molecule inhibitors, developed by Corcept Therapeutics, that selectively target the GR, we have observed marked reduction of growth potential in castration resistant prostate (CRPC) cells dependent upon the AR-V7 isoform and its defined gene signature. We have demonstrated that mifepristone and selective Corcept inhibitors can cooperate with enzalutamide treatment to reduce growth in 22RV1 prostate cancer cells in a dose dependent and synergistic manner. Quantitative PCR analysis demonstrated significant reductions in the ratios of AR-V7 target genes compared to AR full length (AR-FL) target genes, thereby providing a mechanism for improved growth inhibition in Enz resistant prostate cancer cells. These data provide rationale for the clinical co-targeting of AR and GR signaling axes particularly in PC cells with AR isoform dependent progression.