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Recent Advances in the Molecular Biology of Urologic Cancers: Integrative...
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Recent Advances in the Molecular Biology of Urologic Cancers: Integrative Insights from Pathogenesis to Clinical Applications

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 915

Special Issue Editor

Dr. Whi-An Kwon

E-Mail Website
Guest Editor
Department of Urology, Hanyang University College of Medicine, Myongji Hospital, Goyang 10475, Republic of Korea
Interests: urologic oncology; bladder cancer; prostate cancer; immunotherapy; precision medicine; geroscience
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent advances in the molecular biology of urologic cancers, including prostate, renal, and urothelial carcinoma (UC), have paved the way for innovative diagnostic and therapeutic strategies that significantly impact patient outcomes. This Special Issue aims at presenting cutting-edge research and reviews exploring how molecular mechanisms drive tumorigenesis and progression, with an emphasis on translational applications in precision medicine. We invite contributions that address molecular profiling, biomarker discovery, emerging targeted therapies, and the integration of immunotherapeutic approaches. Studies utilizing multi-omics technologies (genomics, transcriptomics, and proteomics) or investigating resistance mechanisms and novel combination regimens are particularly encouraged. By fostering collaboration among basic scientists, clinicians, and industry experts, this collection seeks to accelerate the development of personalized treatment paradigms and improve clinical decision-making. We look forward to receiving your valuable submissions that will broaden our understanding of these complex malignancies and advance patient-centered care.

Dr. Whi-An Kwon
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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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

  • urologic cancers
  • molecular biology
  • pathogenesis
  • precision medicine
  • biomarkers
  • multi-omics
  • targeted therapies
  • immunotherapy
  • translational research
  • clinical applications

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Published Papers (1 paper)

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Research

18 pages, 2778 KB  
Article
High Frequency Loss of 17q11.2 and Downregulation of the Cancer Metastasis Suppression microRNA miR-193a-3p in Prostate Cancer Bone Metastasis
by Elzbieta Stankiewicz, Sarah C. McCarley, Xueying Mao, Sakunthala Kudahetti, Tim Oliver, Jonathan Shamash, Trevor Graham, Daniel M. Berney and Yong-Jie Lu
Cancers 2026, 18(3), 403; https://doi.org/10.3390/cancers18030403 - 27 Jan 2026
Viewed by 544
Abstract
Background/Objectives: Although 90% of prostate cancer (PCa) metastasis occurs in the bone, there are limited studies and rarely available genome-wide profiles at individual sample level for genomic copy number changes in the literature. Methods: We performed Affymetrix SNP 6.0 high-density microarray analysis to [...] Read more.
Background/Objectives: Although 90% of prostate cancer (PCa) metastasis occurs in the bone, there are limited studies and rarely available genome-wide profiles at individual sample level for genomic copy number changes in the literature. Methods: We performed Affymetrix SNP 6.0 high-density microarray analysis to generate the genome-wide copy number change profiles for six cases of PCa bone metastases. A common genomic loss was confirmed by fluorescence in situ hybridization (FISH) in paraffin-embedded PCa bone metastasis samples together with primary PCa and benign prostate hyperplasia samples. We overexpressed the candidate miRNA in PCa cell lines and knocked down its target genes by siRNA transfection and investigated the effect on protein expression and cell viability, migration, and invasion abilities, respectively. Protein expression in PCa tissues was analyzed by immunohistochemical staining. Results: We provided high-resolution PCa bone metastasis profiles of six cases and identified potential bone metastasis-specific common genomic alterations, including a 1.6 mb region on 17q11.2, as well as those shared by non-bone metastatic PCa. The common 17q11.2 loss was confirmed by FISH in further 14/21 PCa bone metastasis samples but was only found in 9/151 primary PCa samples. The well-established tumor-suppressing miRNA located within this small genomic region, miR-193a-3p, was downregulated in both bone metastasis and primary PCa cases, leading to overexpression of cyclin D1 and uPA to promote cancer cell migration and invasion. Cyclin D1 was highly expressed in both localized PCa and bone metastasis samples, and the expression was significantly higher in the latter group (p = 0.013). Conclusions: We generated high-resolution copy number change profiles for bone metastasis samples. This led to the identification of a common, small genomic loss and downregulation of miR-193a-3p, which suppresses PCa bone metastasis through inhibition of its target proteins, providing new insight into bone metastasis development. Full article
(This article belongs to the Special Issue Recent Advances in the Molecular Biology of Urologic Cancers: Integrative Insights from Pathogenesis to Clinical Applications)
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