Castration-Resistant Prostate Cancer: Progress and Promise

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

Deadline for manuscript submissions: 5 December 2024 | Viewed by 1572

Special Issue Editors

Department of Urology, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA
Interests: translational research; castrate-resistant prostate cancer; stem cell and CRPC; cancer cell metabolism; data science; cell signaling; immunotherapy

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Guest Editor
Cleveland Clinic Foundation, Cleveland, OH, USA
Interests: proteomics; translational research; antibody and therapeutic; brain research; neurodegenerative disease; cell signaling; artificial intelligence; immunology
Senior Scientist, Hematology Department, St Jude Children's Research Hospital, Memphis, TN, USA
Interests: cancer; therapeutic development; translational research; cell signaling; immunology

Special Issue Information

Dear Colleagues,

The advanced form of prostate cancer is designated metastatic castration-resistant prostate cancer (mCRPC), which spreads beyond the prostate gland and for which hormone therapy is no longer effective in slowing down disease progression. mCRPC occurs when prostate cancer evolves to resist standard treatment with androgen deprivation therapy (ADT), which blocks the production and signaling activity of hormones called androgens (such as testosterone) that ensure the cancer’s growth. An estimated 50% of diagnosed cases progress to mCRPC within 3 years of diagnosis and this aggressive form of the disease remains lethal despite therapeutic advances. Patients diagnosed with mCRPC have survival ranges from 3 to 78 months. mCRPC remains a clinically challenging late-stage cancer with no curative treatment options. The current treatment options available for mCRPC are the hormonal drugs enzalutamide (brand name XTANDI) and abiraterone (ZYTIGA, which is given with prednisone), which are often used as the first line of therapy for CRPC/mCRPC patients. Moreover, Docetaxel (chemotherapy) is used in patients who are non-responsive to enzalutamide or abiraterone. Recently, the clinical guidelines made some changes in the treatment of CRPC patients; now, mutational testing and the analysis of marker genes such as BRCA2, BRCA1, CHECK2, ATM, and a few others are clinically adaptive to predict the effectiveness of new treatments, including the immune system, In recent years, what has changed in the treatment of mCRPC is that clinical guidelines now include mutational testing and analysis of markers to predict the potential effectiveness of newer treatments that involve immunotherapy.

Dr. Shiv Verma
Dr. Vaibhav Singh
Dr. Man Mohan
Guest Editors

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Keywords

  • castrate-resistant prostate cancer (CRPC)
  • prostate cancer
  • treatment
  • a new therapy
  • drug-resistant
  • marker genes
  • bone metastasis
  • androgen receptor (AR)
  • enzalutamid
  • e abiraterone acetate
  • Docetaxel

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Published Papers (1 paper)

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Research

13 pages, 706 KiB  
Article
Prediction of PSA Response after Dexamethasone Switch during Abiraterone Acetate + Prednisolone Treatment of Metastatic Castration-Resistant Prostate Cancer Patients
by Bertalan Fekete, Krisztina Biró, Fruzsina Gyergyay, Nándor Polk, Orsolya Horváth, Lajos Géczi, Attila Patócs and Barna Budai
Cancers 2024, 16(15), 2760; https://doi.org/10.3390/cancers16152760 - 3 Aug 2024
Viewed by 855
Abstract
Background: The aim was to elaborate a predictive model to find responders for the corticosteroid switch (from prednisolone to dexamethasone) at the first prostate-specific antigen (PSA) progression (≥25% increase) during abiraterone acetate (AA) treatment of metastatic castration-resistant prostate cancer (mCRPC) patients. Methods: If [...] Read more.
Background: The aim was to elaborate a predictive model to find responders for the corticosteroid switch (from prednisolone to dexamethasone) at the first prostate-specific antigen (PSA) progression (≥25% increase) during abiraterone acetate (AA) treatment of metastatic castration-resistant prostate cancer (mCRPC) patients. Methods: If PSA has decreased (≥25%) after switch, patients were considered responders. Logistic regression of 19 dichotomized parameters from routine laboratory and patients’ history was used to find the best model in a cohort of 67 patients. The model was validated in another cohort of 42 patients. Results: The model provided 92.5% and 90.5% accuracy in the testing and the validation cohorts, respectively. Overall the accuracy was 91.7%. The AUC of ROC curve was 0.92 (95% CI 0.85–0.96). After a median follow-up of 27.9 (26.3–84) months, the median AA+dexamethasone treatment duration (TD) in non-responders and responders was 4.7 (3.1–6.5) and 11.1 (8.5–12.9) months and the median overall survival (OS) was 23.2 (15.6–25.8) and 33.5 (26.1–38) months, respectively. Multivariate Cox regression revealed that responsiveness was an independent marker of TD and OS. Conclusions: A high accuracy model was developed for mCRPC patients in predicting cases which might benefit from the switch. For non-responders, induction of the next systemic treatment is indicated. Full article
(This article belongs to the Special Issue Castration-Resistant Prostate Cancer: Progress and Promise)
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