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Cellular cartography reveals mouse prostate organization and determinants of castration resistance.
bioRxiv
December 2024
Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, 48109.
Inadequate response to androgen deprivation therapy (ADT) frequently arises in prostate cancer, driven by cellular mechanisms that remain poorly understood. Here, we integrated single-cell RNA sequencing, single-cell multiomics, and spatial transcriptomics to define the transcriptional, epigenetic, and spatial basis of cell identity and castration response in the mouse prostate. Leveraging these data along with a meta-analysis of human prostates and prostate cancer, we identified cellular orthologs and key determinants of ADT response and resistance.
View Article and Find Full Text PDFIdentification and Validation of Alkaliptosis Resistance-Associated Genes in Prostate Cancer Via Transcriptome Sequencing and Prediction of Biochemical Recurrence.
Mol Biotechnol
January 2025
Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.
Article Synopsis
- Androgen deprivation therapy (ADT) is the main treatment for prostate cancer, but tumors often progress to castration-resistant prostate cancer (CRPC), making it essential to find new therapies.
- Evidence indicates that low oxygen levels (hypoxia) are important for developing CRPC, with the study highlighting the role of alkaliptosis resistance and the marker CA9 in this progression.
- A risk model was created using 12 genes related to alkaliptosis resistance, which correlated strongly with important clinical factors and outcomes like Gleason score, PSA levels, and response to immune therapy.
Prostate ductal adenocarcinoma with MLH1 copy number loss, microsatellite instability high and BRCA2 mutation.
Int Cancer Conf J
January 2025
Department of Urology, The Second Affiliated Hospital of Xi'an Jiaotong University, No. 157 Xiwu Road, Xi'an, 710004 China.
Mismatch repair deficiency (MMRd) or microsatellite instability high (MSI-H) is rare in prostate cancer and more frequently observed in cases with ductal histology. MLH1 copy number loss is extremely rare in MMRd tumors. Herein, we describe a case of prostate ductal adenocarcinoma with MLH1 copy number loss, microsatellite instability high and BRCA2 mutation could derive benefit from immunotherapy plus ADT.
View Article and Find Full Text PDFNeoadjuvant darolutamide plus androgen deprivation therapy for high-risk and locally advanced prostate cancer: a multicenter, open-label, single-arm, phase II trial.
World J Urol
January 2025
Department of Urology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Propose: This study aimed to evaluate the efficacy and safety of neoadjuvant treatment of darolutamide, a next-generation androgen receptor inhibitor, plus androgen deprivation therapy (ADT) for patients with locally advanced prostate cancer (LAPC).
Methods: This single-arm, multicenter, open-label phase II trial (ClinicalTrials.gov: NCT05249712, 2022-01-01), recruited 30 localized high-risk/very high-risk prostate cancer (HRPCa/VHRPCa) patients from three centers in China between 2021 and 2023.
Structurally-oriented classification of FOXA1 alterations identifies prostate cancers with opposing clinical outcomes and distinct molecular and immunologic subtypes.
Clin Cancer Res
January 2025
University of Minnesota, Minneapolis, United States.
Article Synopsis
- This study focused on the diverse types of FOXA1 genetic alterations found in prostate cancer and their implications for clinical management.
- Researchers classified FOXA1 mutations into four distinct classes, each with specific characteristics and prognostic significance based on survival outcomes.
- Results indicated that certain FOXA1 alterations, particularly class 1A, were linked to improved survival rates, while other classes, especially class 2 and amplified versions, were associated with poorer outcomes and higher risks in treatment response.
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