Pub Date : 2024-02-16DOI: 10.1038/s41585-024-00864-0
Annette Fenner
{"title":"Sun, sea, sex and spaghetti as the ESSM hits Bari","authors":"Annette Fenner","doi":"10.1038/s41585-024-00864-0","DOIUrl":"10.1038/s41585-024-00864-0","url":null,"abstract":"","PeriodicalId":19088,"journal":{"name":"Nature Reviews Urology","volume":null,"pages":null},"PeriodicalIF":15.3,"publicationDate":"2024-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139745163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-14DOI: 10.1038/s41585-024-00860-4
Maria Chiara Masone
{"title":"A new rapid point-of-care test for N. gonorrhoeae","authors":"Maria Chiara Masone","doi":"10.1038/s41585-024-00860-4","DOIUrl":"10.1038/s41585-024-00860-4","url":null,"abstract":"","PeriodicalId":19088,"journal":{"name":"Nature Reviews Urology","volume":null,"pages":null},"PeriodicalIF":15.3,"publicationDate":"2024-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41585-024-00860-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139735697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-14DOI: 10.1038/s41585-024-00861-3
Maria Chiara Masone
{"title":"First-morning urine samples to study the urobiome","authors":"Maria Chiara Masone","doi":"10.1038/s41585-024-00861-3","DOIUrl":"10.1038/s41585-024-00861-3","url":null,"abstract":"","PeriodicalId":19088,"journal":{"name":"Nature Reviews Urology","volume":null,"pages":null},"PeriodicalIF":15.3,"publicationDate":"2024-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41585-024-00861-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139735699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-12DOI: 10.1038/s41585-023-00851-x
Lei Yang, Jianming Ying, Qian Tao, Qian Zhang
The N6‐methyladenosine (m6A) modification is the most common modification of messenger RNAs in eukaryotes and has crucial roles in multiple cancers, including in urological malignancies such as renal cell carcinoma, bladder cancer and prostate cancer. The m6A RNA modification is controlled by three types of regulators, including methyltransferases (writers), demethylases (erasers) and RNA‐binding proteins (readers), which are responsible for gene regulation at the post-transcriptional level. This Review summarizes the current evidence indicating that aberrant or dysregulated m6A modification is associated with urological cancer development, progression and prognosis. The complex and context-dependent effects of dysregulated m6A modifications in urological cancers are described, along with the potential for aberrantly expressed m6A regulators to provide valuable diagnostic and prognostic biomarkers as well as new therapeutic targets. RNA m6A modifications have emerged as an important contributor to urological cancer biology. Yang et al. highlight the multifarious roles of m6A modifications and discuss the knowledge gap between molecular understanding and clinical applications.
{"title":"RNA N6-methyladenosine modifications in urological cancers: from mechanism to application","authors":"Lei Yang, Jianming Ying, Qian Tao, Qian Zhang","doi":"10.1038/s41585-023-00851-x","DOIUrl":"10.1038/s41585-023-00851-x","url":null,"abstract":"The N6‐methyladenosine (m6A) modification is the most common modification of messenger RNAs in eukaryotes and has crucial roles in multiple cancers, including in urological malignancies such as renal cell carcinoma, bladder cancer and prostate cancer. The m6A RNA modification is controlled by three types of regulators, including methyltransferases (writers), demethylases (erasers) and RNA‐binding proteins (readers), which are responsible for gene regulation at the post-transcriptional level. This Review summarizes the current evidence indicating that aberrant or dysregulated m6A modification is associated with urological cancer development, progression and prognosis. The complex and context-dependent effects of dysregulated m6A modifications in urological cancers are described, along with the potential for aberrantly expressed m6A regulators to provide valuable diagnostic and prognostic biomarkers as well as new therapeutic targets. RNA m6A modifications have emerged as an important contributor to urological cancer biology. Yang et al. highlight the multifarious roles of m6A modifications and discuss the knowledge gap between molecular understanding and clinical applications.","PeriodicalId":19088,"journal":{"name":"Nature Reviews Urology","volume":null,"pages":null},"PeriodicalIF":12.1,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139720239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-07DOI: 10.1038/s41585-023-00850-y
Ashu Mohammad, Mallory A. Laboulaye, Chen Shenhar, Amy D. Dobberfuhl
Interstitial cystitis/bladder pain syndrome (IC/BPS) is characterized by bladder and/or pelvic pain, increased urinary urgency and frequency and nocturia. The pathophysiology of IC/BPS is poorly understood, and theories include chronic inflammation, autoimmune dysregulation, bacterial cystitis, urothelial dysfunction, deficiency of the glycosaminoglycan (GAG) barrier and urine cytotoxicity. Multiple treatment options exist, including behavioural interventions, oral medications, intravesical instillations and procedures such as hydrodistension; however, many clinical trials fail, and patients experience an unsatisfactory treatment response, likely owing to IC/BPS phenotype heterogeneity and the use of non-targeted interventions. Oxidative stress is implicated in the pathogenesis of IC/BPS as reactive oxygen species impair bladder function via their involvement in multiple molecular mechanisms. Kinase signalling pathways, nociceptive receptors, mast-cell activation, urothelial dysregulation and circadian rhythm disturbance have all been linked to reactive oxygen species and IC/BPS. However, further research is necessary to fully uncover the role of oxidative stress in the pathways driving IC/BPS pathogenesis. The development of new models in which these pathways can be manipulated will aid this research and enable further investigation of promising therapeutic targets. Oxidative stress and reactive oxygen species contribute to the pathophysiology of interstitial cystitis/bladder pain syndrome through their effects on molecular pathways. Here, the authors discuss these pathways, animal models of interstitial cystitis/bladder pain syndrome and treatment options for the disease.
{"title":"Mechanisms of oxidative stress in interstitial cystitis/bladder pain syndrome","authors":"Ashu Mohammad, Mallory A. Laboulaye, Chen Shenhar, Amy D. Dobberfuhl","doi":"10.1038/s41585-023-00850-y","DOIUrl":"10.1038/s41585-023-00850-y","url":null,"abstract":"Interstitial cystitis/bladder pain syndrome (IC/BPS) is characterized by bladder and/or pelvic pain, increased urinary urgency and frequency and nocturia. The pathophysiology of IC/BPS is poorly understood, and theories include chronic inflammation, autoimmune dysregulation, bacterial cystitis, urothelial dysfunction, deficiency of the glycosaminoglycan (GAG) barrier and urine cytotoxicity. Multiple treatment options exist, including behavioural interventions, oral medications, intravesical instillations and procedures such as hydrodistension; however, many clinical trials fail, and patients experience an unsatisfactory treatment response, likely owing to IC/BPS phenotype heterogeneity and the use of non-targeted interventions. Oxidative stress is implicated in the pathogenesis of IC/BPS as reactive oxygen species impair bladder function via their involvement in multiple molecular mechanisms. Kinase signalling pathways, nociceptive receptors, mast-cell activation, urothelial dysregulation and circadian rhythm disturbance have all been linked to reactive oxygen species and IC/BPS. However, further research is necessary to fully uncover the role of oxidative stress in the pathways driving IC/BPS pathogenesis. The development of new models in which these pathways can be manipulated will aid this research and enable further investigation of promising therapeutic targets. Oxidative stress and reactive oxygen species contribute to the pathophysiology of interstitial cystitis/bladder pain syndrome through their effects on molecular pathways. Here, the authors discuss these pathways, animal models of interstitial cystitis/bladder pain syndrome and treatment options for the disease.","PeriodicalId":19088,"journal":{"name":"Nature Reviews Urology","volume":null,"pages":null},"PeriodicalIF":12.1,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139702924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-06DOI: 10.1038/s41585-023-00847-7
Charles C. Guo, Sangkyou Lee, June G. Lee, Huiqin Chen, Michael Zaleski, Woonyoung Choi, David J. McConkey, Peng Wei, Bogdan Czerniak
Bladder cancer is a histologically and clinically heterogenous disease. Most bladder cancers are urothelial carcinomas, which frequently develop distinct histological subtypes. Several urothelial carcinoma histological subtypes, such as micropapillary, plasmacytoid, small-cell carcinoma and sarcomatoid, show highly aggressive behaviour and pose unique challenges in diagnosis and treatment. Comprehensive genomic characterizations of the urothelial carcinoma subtypes have revealed that they probably arise from a precursor subset of conventional urothelial carcinomas that belong to different molecular subtypes — micropapillary and plasmacytoid subtypes develop along the luminal pathway, whereas small-cell and sarcomatoid subtypes evolve along the basal pathway. The subtypes exhibit distinct genomic alterations, but in most cases their biological properties seem to be primarily determined by specific gene expression profiles, including epithelial–mesenchymal transition, urothelial-to-neural lineage plasticity, and immune infiltration with distinct upregulation of immune regulatory genes. These breakthrough studies have transformed our view of bladder cancer histological subtype biology, generated new hypotheses for therapy and chemoresistance, and facilitated the discovery of new therapeutic targets. In this Review, the authors describe the molecular profile of bladder cancer progression associated with the subtypes of this disease and comment on their potential diagnostic, prognostic and therapeutic importance.
{"title":"Molecular profile of bladder cancer progression to clinically aggressive subtypes","authors":"Charles C. Guo, Sangkyou Lee, June G. Lee, Huiqin Chen, Michael Zaleski, Woonyoung Choi, David J. McConkey, Peng Wei, Bogdan Czerniak","doi":"10.1038/s41585-023-00847-7","DOIUrl":"10.1038/s41585-023-00847-7","url":null,"abstract":"Bladder cancer is a histologically and clinically heterogenous disease. Most bladder cancers are urothelial carcinomas, which frequently develop distinct histological subtypes. Several urothelial carcinoma histological subtypes, such as micropapillary, plasmacytoid, small-cell carcinoma and sarcomatoid, show highly aggressive behaviour and pose unique challenges in diagnosis and treatment. Comprehensive genomic characterizations of the urothelial carcinoma subtypes have revealed that they probably arise from a precursor subset of conventional urothelial carcinomas that belong to different molecular subtypes — micropapillary and plasmacytoid subtypes develop along the luminal pathway, whereas small-cell and sarcomatoid subtypes evolve along the basal pathway. The subtypes exhibit distinct genomic alterations, but in most cases their biological properties seem to be primarily determined by specific gene expression profiles, including epithelial–mesenchymal transition, urothelial-to-neural lineage plasticity, and immune infiltration with distinct upregulation of immune regulatory genes. These breakthrough studies have transformed our view of bladder cancer histological subtype biology, generated new hypotheses for therapy and chemoresistance, and facilitated the discovery of new therapeutic targets. In this Review, the authors describe the molecular profile of bladder cancer progression associated with the subtypes of this disease and comment on their potential diagnostic, prognostic and therapeutic importance.","PeriodicalId":19088,"journal":{"name":"Nature Reviews Urology","volume":null,"pages":null},"PeriodicalIF":12.1,"publicationDate":"2024-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139695802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-05DOI: 10.1038/s41585-024-00859-x
Shaun J. Trecarten, Robert S. Svatek
In the SELENIB trial, selenium and vitamin E were compared with placebo as chemoprevention for non-muscle-invasive bladder cancer (NMIBC). No difference versus placebo was observed in recurrence-free interval (RFI) with selenium, but vitamin E was associated with worse RFI. Selenium and vitamin E cannot be recommended in chemoprevention for NMIBC. Furthermore, patients with NMIBC taking supplemental vitamin E should be made aware of its potential association with worse RFI.
在 SELENIB 试验中，硒和维生素 E 作为非肌层浸润性膀胱癌（NMIBC）的化学预防药物与安慰剂进行了比较。与安慰剂相比，硒在无复发间隔期（RFI）方面未观察到差异，但维生素 E 与更差的无复发间隔期有关。在对 NMIBC 进行化学预防时，不能推荐使用硒和维生素 E。此外，应让服用补充维生素 E 的 NMIBC 患者意识到，维生素 E 可能会导致 RFI 下降。
{"title":"Supplementary selenium and vitamin E in non-muscle-invasive bladder cancer","authors":"Shaun J. Trecarten, Robert S. Svatek","doi":"10.1038/s41585-024-00859-x","DOIUrl":"10.1038/s41585-024-00859-x","url":null,"abstract":"In the SELENIB trial, selenium and vitamin E were compared with placebo as chemoprevention for non-muscle-invasive bladder cancer (NMIBC). No difference versus placebo was observed in recurrence-free interval (RFI) with selenium, but vitamin E was associated with worse RFI. Selenium and vitamin E cannot be recommended in chemoprevention for NMIBC. Furthermore, patients with NMIBC taking supplemental vitamin E should be made aware of its potential association with worse RFI.","PeriodicalId":19088,"journal":{"name":"Nature Reviews Urology","volume":null,"pages":null},"PeriodicalIF":12.1,"publicationDate":"2024-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139692463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-02-02DOI: 10.1038/s41585-023-00845-9
Marc Carceles-Cordon, Jacob J. Orme, Josep Domingo-Domenech, Veronica Rodriguez-Bravo
Metastatic prostate cancer remains an incurable lethal disease. Studies indicate that prostate cancer accumulates genomic changes during disease progression and displays the highest levels of chromosomal instability (CIN) across all types of metastatic tumours. CIN, which refers to ongoing chromosomal DNA gain or loss during mitosis, and derived aneuploidy, are known to be associated with increased tumour heterogeneity, metastasis and therapy resistance in many tumour types. Paradoxically, high CIN levels are also proposed to be detrimental to tumour cell survival, suggesting that cancer cells must develop adaptive mechanisms to ensure their survival. In the context of prostate cancer, studies indicate that CIN has a key role in disease progression and might also offer a therapeutic vulnerability that can be pharmacologically targeted. Thus, a comprehensive evaluation of the causes and consequences of CIN in prostate cancer, its contribution to aggressive advanced disease and a better understanding of the acquired CIN tolerance mechanisms can translate into new tumour classifications, biomarker development and therapeutic strategies. Chromosomal instability is a hallmark of advanced prostate cancer. In this Review, the authors discuss the biological causes and paradoxical consequences of chromosomal instability, its potential clinical role in the stratification of prostate cancer aggressiveness and the development of novel treatment strategies.
{"title":"The yin and yang of chromosomal instability in prostate cancer","authors":"Marc Carceles-Cordon, Jacob J. Orme, Josep Domingo-Domenech, Veronica Rodriguez-Bravo","doi":"10.1038/s41585-023-00845-9","DOIUrl":"10.1038/s41585-023-00845-9","url":null,"abstract":"Metastatic prostate cancer remains an incurable lethal disease. Studies indicate that prostate cancer accumulates genomic changes during disease progression and displays the highest levels of chromosomal instability (CIN) across all types of metastatic tumours. CIN, which refers to ongoing chromosomal DNA gain or loss during mitosis, and derived aneuploidy, are known to be associated with increased tumour heterogeneity, metastasis and therapy resistance in many tumour types. Paradoxically, high CIN levels are also proposed to be detrimental to tumour cell survival, suggesting that cancer cells must develop adaptive mechanisms to ensure their survival. In the context of prostate cancer, studies indicate that CIN has a key role in disease progression and might also offer a therapeutic vulnerability that can be pharmacologically targeted. Thus, a comprehensive evaluation of the causes and consequences of CIN in prostate cancer, its contribution to aggressive advanced disease and a better understanding of the acquired CIN tolerance mechanisms can translate into new tumour classifications, biomarker development and therapeutic strategies. Chromosomal instability is a hallmark of advanced prostate cancer. In this Review, the authors discuss the biological causes and paradoxical consequences of chromosomal instability, its potential clinical role in the stratification of prostate cancer aggressiveness and the development of novel treatment strategies.","PeriodicalId":19088,"journal":{"name":"Nature Reviews Urology","volume":null,"pages":null},"PeriodicalIF":15.3,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139659947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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