{"title":"A Novel Molecular Profile of Hormone-Sensitive Prostate Cancer Defines High Risk Patients","authors":"Claudia Piombino, Cecilia Nasso, Stefania Bettelli, Samantha Manfredini, Maria Giuseppa Vitale, Stefania Pipitone, Cinzia Baldessari, Matteo Costantini, Albino Eccher, Ilenia Mastrolia, Virginia Catani, Francesca Bacchelli, Stefania Ferretti, Massimo Dominici, Roberto Sabbatini","doi":"10.1002/cam4.70472","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Background</h3>\n \n <p>The therapeutic management of metastatic hormone-sensitive prostate cancer (mHSPC) is still based on clinical and pathological parameters due to the lack of biomarkers that may drive tailored treatment.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>In this non-randomized, single-center, retrospective trial, we searched for a genetic signature using the NanoString nCounter PanCancer Pathways Panel on formalin-fixed paraffin embedded prostate cancer samples belonging to 48 patients with <i>de novo</i> or relapsed mHSPC. Patients were divided into a high-clinical-risk group (<i>n</i> = 36) and a low-clinical-risk group (<i>n</i>&amp;#x02009;=&amp;#x02009;12) according to the mean time to metastatic relapse.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>The analysis of Nanostring nCounter Panel data revealed differential expression of 42 genes between high-clinical-risk and low-clinical-risk groups. All the genes except for <i>NR4A1</i> and <i>FOS</i> were upregulated in the high-clinical-risk group. A general overexpression of apoptosis, PI3K and MAPK pathway-related genes, including AKT2, was observed in the high-clinical-risk group.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>The differential genetic signature identified between the two study groups revealed novel biomarkers in mHSPC, additionally suggesting new therapeutic targets within the hormone sensitive phase, such as <i>AKT2</i>. Further prospective larger cohort studies are needed to assess the prognostic value of our findings and their exact role in prostate cancer progression.</p>\n </section>\n </div>","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"14 4","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.70472","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Medicine","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/cam4.70472","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background
The therapeutic management of metastatic hormone-sensitive prostate cancer (mHSPC) is still based on clinical and pathological parameters due to the lack of biomarkers that may drive tailored treatment.
Methods
In this non-randomized, single-center, retrospective trial, we searched for a genetic signature using the NanoString nCounter PanCancer Pathways Panel on formalin-fixed paraffin embedded prostate cancer samples belonging to 48 patients with de novo or relapsed mHSPC. Patients were divided into a high-clinical-risk group (n = 36) and a low-clinical-risk group (n&#x02009;=&#x02009;12) according to the mean time to metastatic relapse.
Results
The analysis of Nanostring nCounter Panel data revealed differential expression of 42 genes between high-clinical-risk and low-clinical-risk groups. All the genes except for NR4A1 and FOS were upregulated in the high-clinical-risk group. A general overexpression of apoptosis, PI3K and MAPK pathway-related genes, including AKT2, was observed in the high-clinical-risk group.
Conclusion
The differential genetic signature identified between the two study groups revealed novel biomarkers in mHSPC, additionally suggesting new therapeutic targets within the hormone sensitive phase, such as AKT2. Further prospective larger cohort studies are needed to assess the prognostic value of our findings and their exact role in prostate cancer progression.
期刊介绍:
Cancer Medicine is a peer-reviewed, open access, interdisciplinary journal providing rapid publication of research from global biomedical researchers across the cancer sciences. The journal will consider submissions from all oncologic specialties, including, but not limited to, the following areas:
Clinical Cancer Research
Translational research ∙ clinical trials ∙ chemotherapy ∙ radiation therapy ∙ surgical therapy ∙ clinical observations ∙ clinical guidelines ∙ genetic consultation ∙ ethical considerations
Cancer Biology:
Molecular biology ∙ cellular biology ∙ molecular genetics ∙ genomics ∙ immunology ∙ epigenetics ∙ metabolic studies ∙ proteomics ∙ cytopathology ∙ carcinogenesis ∙ drug discovery and delivery.
Cancer Prevention:
Behavioral science ∙ psychosocial studies ∙ screening ∙ nutrition ∙ epidemiology and prevention ∙ community outreach.
Bioinformatics:
Gene expressions profiles ∙ gene regulation networks ∙ genome bioinformatics ∙ pathwayanalysis ∙ prognostic biomarkers.
Cancer Medicine publishes original research articles, systematic reviews, meta-analyses, and research methods papers, along with invited editorials and commentaries. Original research papers must report well-conducted research with conclusions supported by the data presented in the paper.