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Cancers
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Epigenetics of Prostate Cancer
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Epigenetics of Prostate Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 2842

Special Issue Editor

Dr. Kiran Mahajan

E-Mail Website
Guest Editor
1. Department of Surgery, Cancer Research Building, Washington University in St. Louis, St. Louis, MO 63110, USA
2. Department of Urology, Cancer Research Building, Washington University in St. Louis, St. Louis, MO 63110, USA
3. Siteman Cancer Center, Cancer Research Building, Washington University in St. Louis, St. Louis, MO 63110, USA
Interests: genetic; genomic; molecular and biochemical; novel therapeutics; prostate cancer

Special Issue Information

Dear Colleagues,

I am pleased to invite you to contribute to this Special Issue, the aim of which is to present original research articles, perspectives and reviews that expand our understanding of the epigenetic basis of prostate cancers, how these contribute to metastasis, their resistance to standard of care therapies and the critical roles they play in immune suppression.

A distinguishing feature of prostate cancers is the relatively low mutational burden compared to other cancer types. The disease is driven by epigenetic events at various stages of disease progression. These epigenetic alterations are driven by interactive and dynamic networks involving crosstalk between transcription factors, chromatin remodeling enzymes, kinases, polymerases, ligases, and histones. In addition, the modification of DNA and RNA contributes to epigenomic heterogeneity. Further, alteration in the chromatin landscape results in the expression of nascent non-coding RNAs and formation of pathogenic complexes to promote resistance to various therapies. How these epigenetic changes contribute to immune suppression and lack of response to immune checkpoint blockade therapies is also not well understood. This Special Issue aims to present articles with a focus on epigenetic mechanisms promoting metastasis, and the translational potential of current or novel epigenetic targeted therapies in prostate cancer.

  • Suggested themes and article types for submissions.

In this Special Issue, original research articles, perspectives and reviews are welcome. Research areas may include (but are not limited to) the following:

  • Epigenetic modifications of histones and transcription factors driving prostate cancer.
  • Mechanism-based epigenetic therapies targeting castration resistance.
  • Non-coding RNAs’ mechanism-based understanding of function in prostate cancer progression.
  • Chromatin factors and transcription factors crosstalk in drug resistance.
  • Epigenetics of immune suppression of prostate cancer.
  • Synergy between DNA damage response and epigenetic alterations in recurrence and metastasis.
  • Metabolism-induced epigenetic changes and drug resistance.

I look forward to receiving your contributions.

Dr. Kiran Mahajan
Guest Editor

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 submissions that pass pre-check are 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. Cancers is an international peer-reviewed open access semimonthly 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 2900 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.

Keywords

  • prostate cancer
  • epigenetics
  • castration-resistance
  • metastasis
  • small-molecule therapeutics
  • DNA damage
  • non-coding RNAs
  • immune suppression
  • kinase

Published Papers (2 papers)

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Research

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15 pages, 3601 KiB  
Article
Symptomatic Benign Prostatic Hyperplasia with Suppressed Epigenetic Regulator HOXB13 Shows a Lower Incidence of Prostate Cancer Development
by Nimrod S. Barashi, Tiandao Li, Duminduni H. Angappulige, Bo Zhang, Harry O’Gorman, Charles U. Nottingham, Anup S. Shetty, Joseph E. Ippolito, Gerald L. Andriole, Nupam P. Mahajan, Eric H. Kim and Kiran Mahajan
Cancers 2024, 16(1), 213; https://doi.org/10.3390/cancers16010213 - 02 Jan 2024
Cited by 1 | Viewed by 1482
Abstract
Our objective was to identify variations in gene expression that could help elucidate the pathways for the development of prostate cancer (PCa) in men with Benign Prostatic Hyperplasia (BPH). We included 98 men with BPH, a positive prostate MRI (Prostate Imaging Reporting and [...] Read more.
Our objective was to identify variations in gene expression that could help elucidate the pathways for the development of prostate cancer (PCa) in men with Benign Prostatic Hyperplasia (BPH). We included 98 men with BPH, a positive prostate MRI (Prostate Imaging Reporting and Data System; PIRADS ≥ 4), and a negative biopsy from November 2014 to January 2018. RNA sequencing (RNA-Seq) was performed on tissue cores from the MRI lesion and a geographically distant region (two regions per patient). All patients were followed for at least three years to identify who went on to develop PCa. We compared the gene expressions of those who did not develop PCa (“BPH-only”) vs. those who did (“BPH/PCa”). Then, we identified the subset of men with BPH who had the highest American Urological Association (AUA) symptom scores (“symptomatic BPH”) and compared their gene expression to the BPH/PCa group. At a median follow-up of 47.5 months, 15 men had developed PCa while 83 did not. We compared gene expressions of 14 men with symptomatic BPH (AUAss ≥ 18) vs. 15 with BPH/PCa. We found two clusters of genes, suggesting the two groups had distinctive molecular features. Differential analysis revealed genes that were upregulated in BPH-only and downregulated in BPH/PCa, and vice versa. Symptomatic BPH men had upregulation of T-cell activation markers (TCR, CD3, ZAP70, IL-2 and IFN-γ and chemokine receptors, CXCL9/10) expression. In contrast, men with BPH/PCa had upregulation of NKX3-1 and HOXB13 transcription factors associated with luminal epithelial progenitors but depleted of immune cells, suggesting a cell-autonomous role in immune evasion. Symptomatic BPH with immune-enriched landscapes may support anti-tumor immunity. RNA sequencing of benign prostate biopsy tissue showing upregulation of NKX3-1 and HOXB13 with the absence of T-cells might help in identifying men at higher risk of future PCa development, which may be useful in determining ongoing PCa screening. Full article
(This article belongs to the Special Issue Epigenetics of Prostate Cancer)
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Review

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18 pages, 1263 KiB  
Review
It Takes Two to Tango: The Interplay between Prostate Cancer and Its Microenvironment from an Epigenetic Perspective
by Anniek Zaalberg, Elisabeth Pottendorfer, Wilbert Zwart and Andries M. Bergman
Cancers 2024, 16(2), 294; https://doi.org/10.3390/cancers16020294 - 10 Jan 2024
Viewed by 995
Abstract
Prostate cancer is the second most common cancer in men worldwide and is associated with high morbidity and mortality. Consequently, there is an urgent unmet need for novel treatment avenues. In addition to somatic genetic alterations, deviations in the epigenetic landscape of cancer [...] Read more.
Prostate cancer is the second most common cancer in men worldwide and is associated with high morbidity and mortality. Consequently, there is an urgent unmet need for novel treatment avenues. In addition to somatic genetic alterations, deviations in the epigenetic landscape of cancer cells and their tumor microenvironment (TME) are critical drivers of prostate cancer initiation and progression. Unlike genomic mutations, epigenetic modifications are potentially reversible. Therefore, the inhibition of aberrant epigenetic modifications represents an attractive and exciting novel treatment strategy for castration-resistant prostate cancer patients. Moreover, drugs targeting the epigenome also exhibit synergistic interactions with conventional therapeutics by directly enhancing their anti-tumorigenic properties by “priming” the tumor and tumor microenvironment to increase drug sensitivity. This review summarizes the major epigenetic alterations in prostate cancer and its TME, and their involvement in prostate tumorigenesis, and discusses the impact of epigenome-targeted therapies. Full article
(This article belongs to the Special Issue Epigenetics of Prostate Cancer)
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