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Special Issue "Molecular Research on Urology"

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: closed (30 September 2017)

Special Issue Editors

Guest Editor
Prof. Dr. Jack A. Schalken

Research Director Urology, Dept. of Urology, University Hospital Nijmegen, Box 9101, Nijmegen NL-6500 HB, The Netherlands
Website | E-Mail
Interests: molecular and cellbiology of oncological diseases; cadherine mediated interactions and signal transductions; molecular diagnostics; urogenital oncology; veterinary oncology
Guest Editor
Prof. Dr. Natasha Kyprianou

James F. Hardymon Chair in Urology Research, Professor of Urology, Biochemistry, Pathology and Toxicology & Cancer Biology University of Kentucky College of Medicine, Lexington, KY, United States, United States
Website | E-Mail
Interests: therapeutic approaches for prostate and bladder cancer; molecular pathology of GU malignancies; genetic regulation of apoptosis

Special Issue Information

Dear Colleagues,

Molecular technology platforms have exponentially developed to a status where individual patient-acquired pathologies can be profiled at various levels. Where does the technology meet unmet clinical needs?

In this Special Issue, we invite you to submit manuscripts that illustrate the clinical utility and impact of molecular research into clinical urological practice. We invite both oncological, as well as non-oncological papers. Topics to be considered include, but are not limited to, precision medicine in GU oncology, new molecular therapeutical targets, biomarkers for non-oncological bladder disease, and advances in molecular tissue engineering.

Prof. Dr. Jack A. Schalken
Prof Dr. Natasha Kyprianou
Guest Editors

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.

Keywords

  • Precision medicine in GU oncology
  • New molecular therapeutical targets
  • Biomarkers for non-oncological bladder disease
  • Advances in molecular tissue engineering

Published Papers (11 papers)

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Research

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Open AccessArticle Biofilm Formation by Uropathogenic Escherichia coli Is Favored under Oxygen Conditions That Mimic the Bladder Environment
Int. J. Mol. Sci. 2017, 18(10), 2077; doi:10.3390/ijms18102077
Received: 27 July 2017 / Revised: 15 September 2017 / Accepted: 19 September 2017 / Published: 30 September 2017
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Abstract
One of the most common urologic problems afflicting millions of people worldwide is urinary tract infection (UTI). The severity of UTIs ranges from asymptomatic bacteriuria to acute cystitis, and in severe cases, pyelonephritis and urosepsis. The primary cause of UTIs is uropathogenic Escherichia
[...] Read more.
One of the most common urologic problems afflicting millions of people worldwide is urinary tract infection (UTI). The severity of UTIs ranges from asymptomatic bacteriuria to acute cystitis, and in severe cases, pyelonephritis and urosepsis. The primary cause of UTIs is uropathogenic Escherichia coli (UPEC), for which current antibiotic therapies often fail. UPEC forms multicellular communities known as biofilms on urinary catheters, as well as on and within bladder epithelial cells. Biofilm formation protects UPEC from environmental conditions, antimicrobial therapy, and the host immune system. Previous studies have investigated UPEC biofilm formation in aerobic conditions (21% oxygen); however, urine oxygen tension is reduced (4–6%), and urine contains molecules that can be used by UPEC as alternative terminal electron acceptors (ATEAs) for respiration. This study was designed to determine whether these different terminal electron acceptors utilized by E. coli influence biofilm formation. A panel of 50 urine-associated E. coli isolates was tested for the ability to form biofilm under anaerobic conditions and in the presence of ATEAs. Biofilm production was reduced under all tested sub-atmospheric levels of oxygen, with the notable exception of 4% oxygen, the reported concentration of oxygen within the bladder. Full article
(This article belongs to the Special Issue Molecular Research on Urology)
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Open AccessArticle Dual Strands of Pre-miR-149 Inhibit Cancer Cell Migration and Invasion through Targeting FOXM1 in Renal Cell Carcinoma
Int. J. Mol. Sci. 2017, 18(9), 1969; doi:10.3390/ijms18091969
Received: 31 July 2017 / Revised: 7 September 2017 / Accepted: 7 September 2017 / Published: 13 September 2017
Cited by 1 | PDF Full-text (3853 KB) | HTML Full-text | XML Full-text
Abstract
Our recent studies revealed that dual strands of certain pre-microRNAs, e.g., pre-miR-144, pre-miR-145, and pre-miR-150, act as antitumor microRNAs (miRNAs) in several cancers. The involvement of passenger strands of miRNAs in cancer pathogenesis is a novel concept
[...] Read more.
Our recent studies revealed that dual strands of certain pre-microRNAs, e.g., pre-miR-144, pre-miR-145, and pre-miR-150, act as antitumor microRNAs (miRNAs) in several cancers. The involvement of passenger strands of miRNAs in cancer pathogenesis is a novel concept in miRNA research. The analysis of a miRNA expression signature in clear cell renal cell carcinoma (ccRCC) has revealed that the guide strand of pre-miR-149 is significantly downregulated in cancer tissues. The aims of this study were to investigate the functional significance of miR-149’s guide strand (miR-149-5p) and passenger strand (miR-149-3p), and to identify the oncogenic genes regulated by these miRNAs in ccRCC cells. The ectopic expression of these miRNAs significantly inhibited cancer cell migration and invasion in ccRCC cells. Forkhead box protein M1 (FOXM1) was directly regulated by miR-149-5p and miR-149-3p in ccRCC cells. Knockdown studies using si-FOXM1 showed that the expression of FOXM1 enhanced RCC cell aggressiveness. Interestingly, the analysis of a large number of patients in the The Cancer Genome Atlas (TCGA) database (n = 260) demonstrated that patients with high FOXM1 expression had significantly shorter survival than did those with low FOXM1 expression (p = 1.5 × 10-6). Taken together, dual strands of pre-miR-149 (miR-149-5p and miR-149-3p) acted as antitumor miRNAs through the targeting of FOXM1 in ccRCC cells. Full article
(This article belongs to the Special Issue Molecular Research on Urology)
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Open AccessArticle EpCAM Expression in Lymph Node Metastases of Urothelial Cell Carcinoma of the Bladder: A Pilot Study
Int. J. Mol. Sci. 2017, 18(8), 1802; doi:10.3390/ijms18081802
Received: 17 July 2017 / Revised: 15 August 2017 / Accepted: 16 August 2017 / Published: 18 August 2017
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Abstract
In this retrospective pilot study, the feasibility of the epithelial cell adhesion molecule (EpCAM) as an imaging target for lymph node (LN) metastatic disease of urothelial cell carcinoma (UCC) of the bladder was investigated. LN metastases and LNs without metastases of patients who
[...] Read more.
In this retrospective pilot study, the feasibility of the epithelial cell adhesion molecule (EpCAM) as an imaging target for lymph node (LN) metastatic disease of urothelial cell carcinoma (UCC) of the bladder was investigated. LN metastases and LNs without metastases of patients who underwent pelvic lymph node dissection because of muscle invasive bladder cancer (MIBC) were used. Primary tumors of the same patients were used from cystectomy specimen, transurethral resections, and biopsies. A pathologist, blinded to clinical data, scored EpCAM immunoreactivity. This method determines a total immunostaining score, which is the product of a proportion score and an intensity score. EpCAM expression was observed in 19/20 (95%) LNs with UCC metastases and in 11/12 (92%) of the primary tumors. EpCAM expression was absent in 14/14 (100%) LNs without metastases. Median EpCAM expression (TIS) in LN metastases was 5 (IQR 2.0–8.0) and in the primary tumors 6 (IQR 2.3–11.0). Based on the absence of staining in LNs without metastases, EpCAM show high tumor distinctiveness. EpCAM seems to be a feasible imaging target in LN metastases of UCC of the bladder. Pre- and perioperative visualization of these metastases will improve disease staging and improve the complete resection of LN metastases in MIBC. Full article
(This article belongs to the Special Issue Molecular Research on Urology)
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Open AccessArticle Differential Effects of Histone Acetyltransferase GCN5 or PCAF Knockdown on Urothelial Carcinoma Cells
Int. J. Mol. Sci. 2017, 18(7), 1449; doi:10.3390/ijms18071449
Received: 23 May 2017 / Revised: 26 June 2017 / Accepted: 28 June 2017 / Published: 5 July 2017
PDF Full-text (2873 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Disturbances in histone acetyltransferases (HATs) are common in cancers. In urothelial carcinoma (UC), p300 and CBP are often mutated, whereas the GNAT family HATs GCN5 and PCAF (General Control Nonderepressible 5, p300/CBP-Associated Factor) are often upregulated. Here, we explored the effects of specific
[...] Read more.
Disturbances in histone acetyltransferases (HATs) are common in cancers. In urothelial carcinoma (UC), p300 and CBP are often mutated, whereas the GNAT family HATs GCN5 and PCAF (General Control Nonderepressible 5, p300/CBP-Associated Factor) are often upregulated. Here, we explored the effects of specific siRNA-mediated knockdown of GCN5, PCAF or both in four UC cell lines (UCCs). Expression of various HATs and marker proteins was measured by qRT-PCR and western blot. Cellular effects of knockdowns were analyzed by flow cytometry and ATP-, caspase-, and colony forming-assays. GCN5 was regularly upregulated in UCCs, whereas PCAF was variable. Knockdown of GCN5 or both GNATs, but not of PCAF alone, diminished viability and inhibited clonogenic growth in 2/4 UCCs, inducing cell cycle changes and caspase-3/7 activity. PCAF knockdown elicited GCN5 mRNA upregulation. Double knockdown increased c-MYC and MDM2 (Mouse Double Minute 2) in most cell lines. In conclusion, GCN5 upregulation is especially common in UCCs. GCN5 knockdown impeded growth of specific UCCs, whereas PCAF knockdown elicited minor effects. The limited sensitivity towards GNAT knockdown and its variation between the cell lines might be due to compensatory effects including HAT, c-MYC and MDM2 upregulation. Our results predict that developing drugs targeting individual HATs for UC treatment may be challenging. Full article
(This article belongs to the Special Issue Molecular Research on Urology)
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Open AccessArticle Survivin and NAIP in Human Benign Prostatic Hyperplasia: Protective Role of the Association of Serenoa repens, Lycopene and Selenium from the Randomized Clinical Study
Int. J. Mol. Sci. 2017, 18(3), 680; doi:10.3390/ijms18030680
Received: 30 January 2017 / Revised: 16 March 2017 / Accepted: 17 March 2017 / Published: 22 March 2017
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Abstract
Benign prostatic hyperplasia (BPH) treatment includes the apoptosis machinery modulation through the direct inhibition of caspase cascade. We previously demonstrated that Serenoa repens (Ser) with lycopene (Ly) and selenium (Se) reawakened apoptosis by reducing survivin and neuronal apoptosis inhibitory protein (NAIP) levels in
[...] Read more.
Benign prostatic hyperplasia (BPH) treatment includes the apoptosis machinery modulation through the direct inhibition of caspase cascade. We previously demonstrated that Serenoa repens (Ser) with lycopene (Ly) and selenium (Se) reawakened apoptosis by reducing survivin and neuronal apoptosis inhibitory protein (NAIP) levels in rats. The aim of this study was to evaluate the effectiveness of Ser-Se-Ly association on survivin and NAIP expression in BPH patients. Ninety patients with lower urinary tract symptoms (LUTS) due to clinical BPH were included in this randomized, double-blind, placebo-controlled trial. Participants were randomly assigned to receive placebo (Group BPH + placebo, n = 45) or Ser-Se-Ly association (Group BPH + Ser-Se-Ly; n = 45) for 3 months. At time 0, all patients underwent prostatic biopsies. After 3 months of treatment, they underwent prostatic re-biopsy and specimens were collected for molecular, morphological, and immunohistochemical analysis. After 3 months, survivin and NAIP were significantly decreased, while caspase-3 was significantly increased in BPH patients treated with Ser-Se-Ly when compared with the other group. In BPH patients treated with Ser-Se-Ly for 3 months, the glandular epithelium was formed by a single layer of cuboidal cells. PSA showed high immunoexpression in all BPH patients and a focal positivity in Ser-Se-Ly treated patients after 3 months. Evident prostate specific membrane antigen (PSMA) immunoexpression was shown in all BPH patients, while no positivity was present after Ser-Se-Ly administration. Ser-Se-Ly proved to be effective in promoting apoptosis in BPH patients. Full article
(This article belongs to the Special Issue Molecular Research on Urology)
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Open AccessArticle Serum Metabolomic Profiling Identifies Characterization of Non-Obstructive Azoospermic Men
Int. J. Mol. Sci. 2017, 18(2), 238; doi:10.3390/ijms18020238
Received: 9 November 2016 / Revised: 10 January 2017 / Accepted: 12 January 2017 / Published: 25 January 2017
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Abstract
Male infertility is considered a common health problem, and non-obstructive azoospermia with unclear pathogenesis is one of the most challenging tasks for clinicians. The objective of this study was to investigate the differential serum metabolic pattern in non-obstructive azoospermic men and to determine
[...] Read more.
Male infertility is considered a common health problem, and non-obstructive azoospermia with unclear pathogenesis is one of the most challenging tasks for clinicians. The objective of this study was to investigate the differential serum metabolic pattern in non-obstructive azoospermic men and to determine potential biomarkers related to spermatogenic dysfunction. Serum samples from patients with non-obstructive azoospermia (n = 22) and healthy controls (n = 31) were examined using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Serum metabolomic profiling could differentiate non-obstructive azoospermic patients from healthy control subjects. A total of 24 metabolites were screened and identified as potential markers, many of which are involved in energy production, oxidative stress and cell apoptosis in spermatogenesis. Moreover, the results showed that various metabolic pathways, including d-glutamine and d-glutamate metabolism, taurine and hypotaurine metabolism, pyruvate metabolism, the citrate cycle and alanine, aspartate and glutamate metabolism, were disrupted in patients with non-obstructive azoospermia. Our results indicated that the serum metabolic disorders may contribute to the etiology of non-obstructive azoospermia. This study suggested that serum metabolomics could identify unique metabolic patterns of non-obstructive azoospermia and provide novel insights into the pathogenesis underlying male infertility. Full article
(This article belongs to the Special Issue Molecular Research on Urology)
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Review

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Open AccessReview The Role and Mechanism of Epithelial-to-Mesenchymal Transition in Prostate Cancer Progression
Int. J. Mol. Sci. 2017, 18(10), 2079; doi:10.3390/ijms18102079
Received: 23 August 2017 / Revised: 21 September 2017 / Accepted: 27 September 2017 / Published: 30 September 2017
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Abstract
In prostate cancer (PCa), similar to many other cancers, distant organ metastasis symbolizes the beginning of the end disease, which eventually leads to cancer death. Many mechanisms have been identified in this process that can be rationalized into targeted therapy. Among them, epithelial-to-mesenchymal
[...] Read more.
In prostate cancer (PCa), similar to many other cancers, distant organ metastasis symbolizes the beginning of the end disease, which eventually leads to cancer death. Many mechanisms have been identified in this process that can be rationalized into targeted therapy. Among them, epithelial-to-mesenchymal transition (EMT) is originally characterized as a critical step for cell trans-differentiation during embryo development and now recognized in promoting cancer cells invasiveness because of high mobility and migratory abilities of mesenchymal cells once converted from carcinoma cells. Nevertheless, the underlying pathways leading to EMT appear to be very diverse in different cancer types, which certainly represent a challenge for developing effective intervention. In this article, we have carefully reviewed the key factors involved in EMT of PCa with clinical correlation in hope to facilitate the development of new therapeutic strategy that is expected to reduce the disease mortality. Full article
(This article belongs to the Special Issue Molecular Research on Urology)
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Open AccessReview Tissue-Based MicroRNAs as Predictors of Biochemical Recurrence after Radical Prostatectomy: What Can We Learn from Past Studies?
Int. J. Mol. Sci. 2017, 18(10), 2023; doi:10.3390/ijms18102023
Received: 18 August 2017 / Revised: 16 September 2017 / Accepted: 19 September 2017 / Published: 21 September 2017
Cited by 1 | PDF Full-text (984 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
With the increasing understanding of the molecular mechanism of the microRNAs (miRNAs) in prostate cancer (PCa), the predictive potential of miRNAs has received more attention by clinicians and laboratory scientists. Compared with the traditional prognostic tools based on clinicopathological variables, including the prostate-specific
[...] Read more.
With the increasing understanding of the molecular mechanism of the microRNAs (miRNAs) in prostate cancer (PCa), the predictive potential of miRNAs has received more attention by clinicians and laboratory scientists. Compared with the traditional prognostic tools based on clinicopathological variables, including the prostate-specific antigen, miRNAs may be helpful novel molecular biomarkers of biochemical recurrence for a more accurate risk stratification of PCa patients after radical prostatectomy and may contribute to personalized treatment. Tissue samples from prostatectomy specimens are easily available for miRNA isolation. Numerous studies from different countries have investigated the role of tissue-miRNAs as independent predictors of disease recurrence, either alone or in combination with other clinicopathological factors. For this purpose, a PubMed search was performed for articles published between 2008 and 2017. We compiled a profile of dysregulated miRNAs as potential predictors of biochemical recurrence and discussed their current clinical relevance. Because of differences in analytics, insufficient power and the heterogeneity of studies, and different statistical evaluation methods, limited consistency in results was obvious. Prospective multi-institutional studies with larger sample sizes, harmonized analytics, well-structured external validations, and reasonable study designs are necessary to assess the real prognostic information of miRNAs, in combination with conventional clinicopathological factors, as predictors of biochemical recurrence. Full article
(This article belongs to the Special Issue Molecular Research on Urology)
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Open AccessReview Tyrosine-Kinase Inhibitors Therapies with Mainly Anti-Angiogenic Activity in Advanced Renal Cell Carcinoma: Value of PET/CT in Response Evaluation
Int. J. Mol. Sci. 2017, 18(9), 1937; doi:10.3390/ijms18091937
Received: 19 August 2017 / Revised: 5 September 2017 / Accepted: 6 September 2017 / Published: 9 September 2017
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Abstract
Renal cell carcinoma (RCC) is the most frequent renal tumor and the majority of patients are diagnosed with advanced disease. Tumor angiogenesis plays a crucial role in the development and progression of RCC together with hypoxia and glucose metabolism. These three pathways are
[...] Read more.
Renal cell carcinoma (RCC) is the most frequent renal tumor and the majority of patients are diagnosed with advanced disease. Tumor angiogenesis plays a crucial role in the development and progression of RCC together with hypoxia and glucose metabolism. These three pathways are strictly connected to the cell growth and proliferation, like a loop that is self-feeding. Over the last few years, the ever-deeper knowledge of its contribution in metastatic RCC led to the discovery of numerous tyrosine kinase inhibitors (TKIs) targeting pro-angiogenic receptors at different levels such as sunitinib, sorafenib, pazopanib, axitinib, tivozanib, and dovitinib. As anti-angiogenic agents, TKIs interfere the loop, being able to inhibit tumor proliferation. TKIs are now available treatments for advanced RCC, which demonstrated to improve overall survival and/or progression free survival. Their effects can be detectable early on Positron Emission Tomography/Computed Tomography (PET/CT) by change in 18F-fluoro-2-deoxy-2-d-glucose (18F-FDG) uptake, the main radiotracer used to date, as a strong indicator of biological response. 18F-FDG PET/CT demonstrated an ability to predict and monitor disease progression, allowing an early and reliable identification of responders, and could be used for image-guided optimization and “personalization” of anti-angiogenic regimens. New radiotracers for biometabolic imaging are currently under investigation, which exploit the other pathways involved in the cancer process, including cellular proliferation, aerobic metabolism, cell membrane synthesis, hypoxia and amino acid transport, as well as the angiogenic process, but they require further studies. Full article
(This article belongs to the Special Issue Molecular Research on Urology)
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Open AccessReview Neuroprotective and Nerve Regenerative Approaches for Treatment of Erectile Dysfunction after Cavernous Nerve Injury
Int. J. Mol. Sci. 2017, 18(8), 1794; doi:10.3390/ijms18081794
Received: 20 July 2017 / Revised: 10 August 2017 / Accepted: 12 August 2017 / Published: 18 August 2017
PDF Full-text (785 KB) | HTML Full-text | XML Full-text
Abstract
Erectile dysfunction (ED) is a significant cause of reduced quality of life in men and their partners. Cavernous nerve injury (CNI) during pelvic surgery results in ED in greater than 50% of patients, regardless of additional patient factors. ED related to CNI is
[...] Read more.
Erectile dysfunction (ED) is a significant cause of reduced quality of life in men and their partners. Cavernous nerve injury (CNI) during pelvic surgery results in ED in greater than 50% of patients, regardless of additional patient factors. ED related to CNI is difficult to treat and typically poorly responsive to first- and second-line therapeutic options. Recently, a significant amount of research has been devoted to exploring neuroprotective and neuroregenerative approaches to salvage erectile function in patients with CNI. In addition, therapeutic options such as neuregulins, immunophilin ligands, gene therapy, stem cell therapy and novel surgical strategies, have shown benefit in pre-clinical, and limited clinical studies. In the era of personalized medicine, these new therapeutic technologies will be the future of ED treatment and are described in this review. Full article
(This article belongs to the Special Issue Molecular Research on Urology)
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Open AccessReview Advances in Understanding of Penile Carcinogenesis: The Search for Actionable Targets
Int. J. Mol. Sci. 2017, 18(8), 1777; doi:10.3390/ijms18081777
Received: 1 August 2017 / Revised: 13 August 2017 / Accepted: 14 August 2017 / Published: 16 August 2017
Cited by 1 | PDF Full-text (781 KB) | HTML Full-text | XML Full-text
Abstract
Penile cancer (PeCa) is a rare malignancy with potentially devastating effects. Squamous cell carcinoma is the most common variant with distinct precancerous lesions before development into invasive disease. Involvement of the inguinal lymph nodes is the most important prognostic factor in PeCa, and
[...] Read more.
Penile cancer (PeCa) is a rare malignancy with potentially devastating effects. Squamous cell carcinoma is the most common variant with distinct precancerous lesions before development into invasive disease. Involvement of the inguinal lymph nodes is the most important prognostic factor in PeCa, and once disease is present outside the groin, prognosis is poor. Metastatic PeCa is challenging to treat and often requires multidisciplinary approaches in management. Due to its rarity, molecular understanding of the disease continues to be limited with most studies based on small, single center series. Thus far, it appears PeCa has diverse mechanisms of carcinogenesis affecting similar molecular pathways. In this review, we evaluate the current landscape of the molecular carcinogenesis of PeCa and explore ongoing research on potential actionable targets of therapy. The emergence of anti-epidermal growth factor receptor (EGFR) and other immunotherapeutic strategies may improve outcomes for PeCa patients. Full article
(This article belongs to the Special Issue Molecular Research on Urology)
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