bims-meproc 2025-05-18 papers

bims-meproc

Biomed News

on Metabolism in Prostate Cancer

Issue of 2025–05–18
twelve papers selected by
Grigor Varuzhanyan, UCLA

New insights into gut microbiota-prostate cancer crosstalk.
GLP-1 Agonist Use Among Men with Localized Prostate Cancer: A Narrative Review and Rationale for Prospective Clinical Trials.
Mitochondrial HSP90 paralog TRAP1 deletion drives glutamine addiction in tumor cells via destablization of the Cys/Glu antiporter SLC7A11/xCT.
Metabolic Plasticity in Prostate Cancer: The Warburg Effect and Its Clinical Relevance.
Development and validation of tryptophan metabolism-related risk model and molecular subtypes for predicting postoperative biochemical recurrence in prostate cancer.
The Emerging Oncogenic Role of RARγ: From Stem Cell Regulation to a Potential Cancer Therapy.
Inhibition of Mitochondrial-Associated Protein MAGMAS Resensitizes Chemoresistant Prostate Cancer Cells to Docetaxel.
Development of a machine learning-based predictive risk model combining fatty acid metabolism and ferroptosis for immunotherapy response and prognosis in prostate cancer.
CHD1 loss reprograms SREBP2-driven cholesterol synthesis to fuel androgen-responsive growth and castration resistance in SPOP-mutated prostate tumors.
Single-Cell Profiling of Mononuclear Cells Identifies Transcriptomics Signatures Differentiating Prostate Cancer From Benign Prostatic Hyperplasia.
7,7-Bis(3-Indolyl)-p-Cresol, a Metabolite from Marine-Derived Bacterium Vibrio spp. DJA11, Suppresses the Proliferation and Motility of Prostate Cancer Cells.
Mitochondrial DNA copy number assessment is a potent predictor for prostate cancer in White but not Black Individuals.

Trends Mol Med. 2025 May 06. pii: S1471-4914(25)00087-5. [Epub ahead of print]

New insights into gut microbiota-prostate cancer crosstalk.

Jalal Laaraj, Gabriel Lachance, Alain Bergeron, Yves Fradet, Karine Robitaille, Vincent Fradet.

  Recent evidence underscores a reciprocal relationship between the gut microbiota and prostate cancer (PCa). Dysbiosis, often driven by Western dietary habits and antibiotic use, can heighten systemic inflammation and hinder antitumor immunity, thereby fostering PCa onset and progression. Conversely, certain gut microbes and their metabolites may protect against tumor growth by modulating immune and hormonal pathways that impact therapeutic responses, including androgen deprivation therapy (ADT). Emerging evidence links gut microbial shifts to PCa aggressiveness, potentially sustaining local androgen production and promoting resistance. In this review, we explore current understanding of the gut-PCa interplay, highlighting key knowledge gaps and the need for further research to clarify how targeting the microbiome might influence PCa outcomes.

Keywords:  Western dietary habits; dysbiosis; gut microbiota,; gut-derived metabolites; immunotherapy; prostate cancer

DOI:  https://doi.org/10.1016/j.molmed.2025.03.015
Urology. 2025 May 08. pii: S0090-4295(25)00426-1. [Epub ahead of print]

GLP-1 Agonist Use Among Men with Localized Prostate Cancer: A Narrative Review and Rationale for Prospective Clinical Trials.

Andrew Fang, Daniel E Frigo, Andrew Hahn, Zayd Razouki, Jessica Hwang, Efstratios Koutroumpakis, Tarek Lawen, Matthew Smith, Jill Hamilton-Reeves, John DiGiovanni, Noel Higgason, Rebekka S Garcia, Brian F Chapin, Curtis Pettaway, Lisly Chery, Patricia Troncoso, Christopher Logothetis, Carrie R Daniel, Peng Wei, Justin R Gregg.

  GLP-1 receptor agonists are a revolutionary treatment for obesity and investigations into other uses of these agents are ongoing. Epidemiologic data suggest that prostate cancer risk may decrease following GLP-1 receptor agonist initiation. To better define the potential role of GLP-1 receptor agonist use among men with prostate cancer, we will define changes that occur in men with prostate cancer following lifestyle intervention; illuminate the current relationship between these interventions and prostate cancer risk; and explore the potential mechanism of action on tumor biology, providing rationale for evaluating its effects on prostate cancer in a planned clinical trial.

Keywords:  GLP-1/GIP RA; Lifestyle intervention; prostate cancer

DOI:  https://doi.org/10.1016/j.urology.2025.04.056
Mol Cancer Res. 2025 May 16.

Mitochondrial HSP90 paralog TRAP1 deletion drives glutamine addiction in tumor cells via destablization of the Cys/Glu antiporter SLC7A11/xCT.

Abhinav Joshi, Li Dai, Marisa Maisiak, Sunmin Lee, Elizabeth Lopez, Takeshi Ito, Len Neckers.

TRAP1, the mitochondrial isoform of HSP90, has emerged as a key regulator of cancer cell metabolism, yet the mechanisms by which it rewires nutrient utilization remain poorly understood. We previously reported that TRAP1 loss increases glutamine dependency of mitochondrial respiration following glucose withdrawal. Here, we investigate how TRAP1 deletion impacts glucose metabolism and the mechanisms enabling glutamine retention to support mitochondrial respiration via reductive carboxylation and the oxidative TCA cycle. TRAP1 knockout (KO) in bladder and prostate cancer cells recapitulates the carbon source-specific metabolic rewiring previously observed. Stable isotope tracing reveals that although glucose oxidation remains functional, TRAP1 KO reduces overall glucose uptake and its contribution to glycolysis and the pentose phosphate pathway. This effect is consistent across multiple cell lines. Concurrently, TRAP1-deficient cells exhibit increased glutamine retention and reliance, potentially due to downregulation of the cystine/glutamate antiporter SLC7A11/xCT. Supporting this, xCT overexpression reduces glutamine-dependent respiration in TRAP1 KO cells. qPCR and proteasome inhibition assays suggest xCT is regulated post-translationally via protein stability. Notably, xCT suppression does not trigger ferroptosis, indicating a selective adaptation rather than induction of cell death. Together, our findings suggest that TRAP1 loss decreases glucose uptake while preserving its metabolic fate, promoting glutamine conservation through xCT downregulation to maintain mitochondrial respiration without inducing ferroptosis. Implications: These results reveal a TRAP1-dependent mechanism of metabolic rewiring in cancer cells and identify xCT-mediated glutamine conservation as a key adaptive response, underscoring TRAP1 as a potential metabolic vulnerability and therapeutic target in tumors with altered nutrient utilization.

DOI: https://doi.org/10.1158/1541-7786.MCR-24-0194
Am J Clin Oncol. 2025 May 15.

Metabolic Plasticity in Prostate Cancer: The Warburg Effect and Its Clinical Relevance.

Arielle Sabbah, Guila Delouya, Mikhael Laskine, Daniel Taussky.

   OBJECTIVES: This paper examines the life and research of Otto Warburg (1883 to 1970), who identified the so-called Warburg effect. Warburg personal life and scientific career were notable.
METHODS: This study summarizes the key aspects of his life, the Warburg effect, and its significance in prostate cancer.
RESULTS: Despite being classified as non-Aryan, Warburg continued his research as the director of the Kaiser Wilhelm Institute for Cell Physiology during World War II. He also cohabited openly with a male partner. The Warburg effect is a metabolic hallmark of cancer, where cells preferentially utilize glycolysis over oxidative phosphorylation, even in the presence of oxygen. This metabolic shift confers key advantages to tumor survival, including rapid ATP production, biosynthetic support for proliferation, and resistance to apoptosis. In prostate cancer, the metabolism undergoes a unique transformation. Normal prostate cells are characterized by citrate secretion; however, as malignancy develops, the cells adapt to oxidative metabolism. At the metastatic stage, the Warburg effect becomes more pronounced and is influenced by the tumor microenvironment and interactions with cancer-associated fibroblasts and bone marrow adipocytes. These metabolic changes have significant clinical implications. While FDG-PET scans serve as a diagnostic tool in many cancers, their utility in early-stage prostate cancer is limited owing to its delayed metabolic shift. Metabolic-targeted therapies, such as dichloroacetate (DCA) and glycolysis inhibitors, are emerging as promising strategies to enhance the efficacy of chemotherapy and radiotherapy.
CONCLUSIONS: Elucidating the role of metabolic reprogramming in prostate cancer could reveal new avenues for treatment, particularly for castration-resistant and metastatic diseases.

Keywords:  Warburg effect; glycolysis inhibitors; metabolic changes; metabolic-targeted therapies; prostate cancer

DOI:  https://doi.org/10.1097/COC.0000000000001215
Transl Androl Urol. 2025 Apr 30. 14(4): 1082-1110

Development and validation of tryptophan metabolism-related risk model and molecular subtypes for predicting postoperative biochemical recurrence in prostate cancer.

Yuan Shao, Xiaolei Zhang, Yinchi Zhang, Zihao Liu, Zhen Yang, Yang Liu, Hua Huang, Zeyuan Wang, Zhinan Fu, Yong Wang.

   Background: Biochemical recurrence (BCR) following radical prostatectomy (RP) remains a major challenge in prostate cancer (PCa) management. Tryptophan metabolism plays a pivotal role in tumor progression and immune modulation. This study aimed to develop and validate a tryptophan metabolism-related risk model and molecular subtypes to predict BCR in PCa patients after RP.
Methods: The Cancer Genome Atlas-Prostate Adenocarcinoma (TCGA-PRAD) dataset, including 421 PCa patients, was analyzed to identify key tryptophan metabolism-related genes (TMRGs) using differential expression, univariate Cox, and the least absolute shrinkage and selection operator (LASSO) regression analyses. The tryptophan metabolism-related risk model was constructed through multivariate Cox regression, and tryptophan metabolism-related molecular subtypes were established using consensus clustering. External validation was conducted using an independent dataset, while immunohistochemistry (IHC) and single-cell sequencing further confirmed TMRG expression patterns and their roles in the tumor microenvironment (TME).
Results: The tryptophan metabolism-related risk model and molecular subtypes effectively stratified PCa patients into low- and high-risk groups or two molecular subtypes. High-risk PCa patients (n=211) and those in Cluster 1 (n=261) exhibited significantly poorer biochemical recurrence-free survival (BRFS) and distinct clinicopathological features, immune infiltration profiles, and TME characteristics. External validation confirmed the robustness of the tryptophan metabolism-related risk model and molecular subtypes. IHC and single-cell sequencing highlighted the expression patterns of TMRGs and their regulatory roles in the TME.
Conclusions: This study established and validated tryptophan metabolism-related risk scores and molecular subtypes as reliable predictors of BCR in PCa patients after RP. These findings provide a foundation for personalized follow-up and treatment strategies, contributing to improved clinical outcomes in PCa management.

Keywords:  Prostate cancer (PCa); biochemical recurrence (BCR); molecular subtypes; risk model; tryptophan

DOI:  https://doi.org/10.21037/tau-2025-39
Int J Mol Sci. 2025 May 03. pii: 4357. [Epub ahead of print]26(9):

The Emerging Oncogenic Role of RARγ: From Stem Cell Regulation to a Potential Cancer Therapy.

Geoffrey Brown.

  Retinoic acid receptor (RAR) γ expression is restricted during adult haematopoiesis to haematopoietic stem cells and their immediate offspring and is required for their maintenance. From zebrafish studies, RARγ is selectively expressed by stem cells and agonism in the absence of exogenous all-trans retinoic acid blocked stem cell development. Recent findings for the expression of RARγ have revealed an oncogenic role in acute myeloid leukaemia and cholangiocarcinoma and colorectal, head and neck, hepatocellular, ovarian, pancreatic, prostate, and renal cancer. Overexpression and agonism of RARγ enhanced cell proliferation for head and neck, hepatocellular, and prostate cancer. RARγ antagonism, pan-RAR antagonism, and RARγ downregulation led to cell growth which was often followed by cell death for acute myeloid leukaemia, astrocytoma, and cholangiocarcinoma as well as hepatocellular, primitive, neuroectodermal ovarian, and prostate cancer. Histological studies have associated high level RARγ expression with high-grade disease, metastasis, and a poor prognosis for cholangiocarcinoma and ovarian, pancreatic, and prostate cancer. RARγ is expressed by cancer stem cells and is a targetable drive of cancer cell growth and survival.

Keywords:  cancer stem cells; carcinoma; cell development; normal stem cells; retinoic acid receptor γ; therapeutics

DOI:  https://doi.org/10.3390/ijms26094357
Cancers (Basel). 2025 Apr 30. pii: 1535. [Epub ahead of print]17(9):

Inhibition of Mitochondrial-Associated Protein MAGMAS Resensitizes Chemoresistant Prostate Cancer Cells to Docetaxel.

Alfonso M Durán, Kristen Whitley, Krystal Santiago, Christian Yoo, Giancarlo Valdez, Kai Wen Cheng, Pedro Ochoa, David de Semir, Joanne Xiu, Parthiban Chokkalingam, Sasmita Das, Eric S Schaefer, Steven P Rowe, Bhaskar C Das, Carlos A Casiano, Frankis Almaguel.

   BACKGROUND/OBJECTIVES: Metastatic prostate cancer (PCa) is the leading cause of cancer-related deaths and a major contributor to cancer mortality in men. Most patients with metastatic PCa eventually develop metastatic castration-resistant prostate cancer (mCRPC), characterized by resistance to treatment with androgen-deprivation therapy, and often later the development of resistance to other types of agents. MAGMAS, a 13.8 kDa mitochondrial-associated protein, facilitates the import of nuclear-encoded proteins into the mitochondrial matrix. Overexpression of MAGMAS has been observed in several aggressive cancers, including breast, glioblastoma, and prostate cancer. When overexpressed, MAGMAS acts as a cytoprotective protein by scavenging reactive oxygen species (ROS), maintaining ROS levels that support cell proliferation while avoiding the induction of apoptosis. This study investigates the role of MAGMAS in therapy resistance in PCa cells.
METHODS/RESULTS: Quantitative immunoblotting revealed that MAGMAS is endogenously upregulated in docetaxel-resistant (DR) PCa cell lines compared to their docetaxel-sensitive parental counterparts. While MAGMAS depletion alone did not affect the survival of DR cells, it significantly sensitized them to docetaxel (DTX), as indicated by a marked reduction in clonogenic potential. Additionally, transient knockdown of MAGMAS in these resistant cells significantly decreased the levels of ABCB1 protein. Consistent with these findings, sub-therapeutic inhibition of MAGMAS using the novel BT#9 inhibitor, in combination with increasing concentrations of DTX, enhanced the sensitivity of DR cells to DTX, as demonstrated by proliferation and clonogenic assays. Lastly, RNA tumor expression predicts overall survival (OS).
CONCLUSIONS: These results implicate MAGMAS in PCa chemoresistance and suggest that targeting this protein could provide a novel therapeutic strategy for treating DR tumors.

Keywords:  MAGMAS; chemoresistance; docetaxel; mitochondria; prostate cancer

DOI:  https://doi.org/10.3390/cancers17091535
Discov Oncol. 2025 May 13. 16(1): 744

Development of a machine learning-based predictive risk model combining fatty acid metabolism and ferroptosis for immunotherapy response and prognosis in prostate cancer.

Zhenwei Wang, Zhihong Dai, Yuren Gao, Zhongxiang Zhao, Zhen Li, Liang Wang, Xiang Gao, Qiuqiu Qiu, Xiaofu Qiu, Zhiyu Liu.

  Prostate cancer (PCa) remains a leading cause of cancer-related mortality, necessitating robust prognostic models and personalized therapeutic strategies. This study integrated bulk RNA sequencing, single-cell RNA sequencing (scRNA-seq), and spatial transcriptomics to construct a prognostic model based on genes shared between ferroptosis and fatty acid metabolism (FAM). Using the TCGA-PRAD dataset, we identified 73 differentially expressed genes (DEGs) at the intersection of ferroptosis and FAM, of which 19 were significantly associated with progression-free survival (PFS). A machine learning-based prognostic model, optimized using the Lasso + Random Survival Forest (RSF) algorithm, achieved a high C-index of 0.876 and demonstrated strong predictive accuracy (1-, 2-, and 3-year AUCs: 0.77, 0.75, and 0.78, respectively). The model, validated in the DFKZ cohort, stratified patients into high- and low-risk groups, with the high-risk group exhibiting worse PFS and higher tumor mutation burden (TMB). Functional enrichment analysis revealed distinct pathway activities, with high-risk patients showing enrichment in immune-related and proliferative pathways, while low-risk patients were enriched in metabolic pathways. Immune microenvironment analysis revealed heightened immune activity in high-risk patients, characterized by increased infiltration of CD8 + T cells, regulatory T cells, and M2 macrophages, alongside elevated TIDE scores, suggesting immune evasion and resistance to immunotherapy. In contrast, low-risk patients exhibited higher infiltration of plasma cells and neutrophils and demonstrated better responses to immune checkpoint inhibitors (ICIs). Spatial transcriptomics and scRNA-seq further elucidated the spatial distribution of model genes, highlighting the central role of macrophages in mediating risk stratification. Additionally, chemotherapy sensitivity analysis identified potential therapeutic agents, such as Erlotinib and Picolinic acid, for low-risk patients. In vitro experiments showed that overexpression of CD38 in the PC-3 cell line led to elevated lipid peroxidation (C11-BODIPY) and reactive oxygen species (ROS), suggesting increased cell ferroptosis. These findings provide a comprehensive framework for risk stratification and personalized treatment in PCa, bridging molecular mechanisms with clinical outcomes.

Keywords:  Fatty acid metabolism; Ferroptosis; Machine learning; Multi-omics; Prostate cancer; Tumor microenvironment

DOI:  https://doi.org/10.1007/s12672-025-02484-5
Nat Cancer. 2025 May 13.

CHD1 loss reprograms SREBP2-driven cholesterol synthesis to fuel androgen-responsive growth and castration resistance in SPOP-mutated prostate tumors.

Feiyu Chen, Haoyan Li, Yin Wang, Ximing Tang, Kevin Lin, Qidong Li, Chenling Meng, Wei Shi, Javier Leo, Xin Liang, Jie Zhang, Vivien Van, Iqbal Mahmud, Bo Wei, Philip L Lorenzi, Maria G Raso, Ana Aparicio, Yue Lu, Daniel E Frigo, Boyi Gan, Di Zhao.

Despite undergoing castration, most individuals with prostate cancer (PCa) experience progression to castration-resistant PCa (CRPC), in which the androgen receptor (AR) remains an important driver. Concurrent genetic alterations in SPOP and CHD1 define a unique subtype of PCa, but their interactions in tumor progression and therapy response remain unclear. Here, we provide genetic evidence supporting that CHD1 loss accelerates disease progression and confers resistance to castration in males with SPOP-mutated PCa. By leveraging genetic engineering and multiomics, we uncovered a noncanonical function of CHD1 in lipid metabolism reprogramming via repressing the SREBP2 transcriptome. Loss of CHD1 induces cholesterol production, supplies intratumoral androgen biosynthesis and enhances AR activity, leading to castration resistance of SPOP-mutated PCa. Combining anti-androgen therapy with cholesterol-lowering drugs showed synergistic and durable activity against CRPC harboring CHD1 loss and SPOP mutations. These findings advance our understanding of an emerging PCa subtype and offer biomarker-driven combinatorial treatment strategies for men with CRPC.

DOI: https://doi.org/10.1038/s43018-025-00952-z
Genes Chromosomes Cancer. 2025 May;64(5): e70051

Single-Cell Profiling of Mononuclear Cells Identifies Transcriptomics Signatures Differentiating Prostate Cancer From Benign Prostatic Hyperplasia.

Kadriia Enikeeva, Vyacheslav Korobeynikov, Yuliya Sharifyanova, Elina Akramova, Polina Shmelkova, Diana Gainullinа, Liliia Kalimullina, Valentin Pavlov.

  Prostate cancer (PCa) and benign prostatic hyperplasia (BPH) share overlapping etiological factors but differ molecularly. In the study, 4 patients with prostate cancer and 3 patients with BPH were included. All patients with prostate cancer and BPH had a histologically confirmed diagnosis. Among the prostate cancer group were 3 patients with acinar prostate adenocarcinoma and 1 patient with small-acinar prostate adenocarcinoma. Using single-cell RNA sequencing (scRNA-seq) on peripheral blood mononuclear cells (PBMCs) from PCa and BPH patients, we identified 16 immune cell clusters, with elevated CD14+ monocytes, NK cells, and γδ T cells in PCa. Differential gene expression analysis revealed 40 overexpressed genes in PCa monocytes, including CSMD1, ZBTB16, ZNF217, and SERPINI2, linked to tumor progression, cell cycle regulation, EMT, androgen signaling, and metabolism. SCN2A was highly expressed in PCa B cells, while ABO, FMN1, and TXNIP in CD4+ T cells modulated immune evasion, cytoskeletal regulation, and oxidative stress. Pathway analysis showed PCa monocytes had heightened interleukin-27 signaling, whereas BPH monocytes exhibited increased cholesterol storage and Notch signaling. CellChat analysis highlighted monocytes' central role in immune regulation, with distinct interactions via MIF, galectin, and TGF-β pathways in PCa and BPH. These findings reveal unique immune microenvironments and transcriptional heterogeneity between PCa and BPH, offering potential biomarkers for differentiation and insights into prostate pathology mechanisms.

Keywords:  benigh prostatic hyperplasia; prostate cancer; single‐cell sequencing; transcriptome

DOI:  https://doi.org/10.1002/gcc.70051
J Microbiol Biotechnol. 2025 May 15. 35 e2502035

7,7-Bis(3-Indolyl)-p-Cresol, a Metabolite from Marine-Derived Bacterium Vibrio spp. DJA11, Suppresses the Proliferation and Motility of Prostate Cancer Cells.

Sultan Pulat, Eun-Young Lee, Grace Choi, Yoon-Hee Jung, Sang-Jip Nam, Hangun Kim.

  Bacteria such as Vibrio spp. in the marine environment can produce secondary metabolites which have significant potential applications in pharmaceuticals. In a study to discover bioactive secondary metabolites from marine Vibrio spp., the strain DJA11 was encountered. HPLC/UV-guided isolation of the crude extract from this strain has led to the discovery of compound 1. Prostate cancer (PCa) is one of the biggest worldwide health issues because of its high diagnosis. CWR22Rv1 (22Rv1) is mutated in WT p53 and AR, C4-2 is derived from androgen-dependent human LNCaP and PC-3 is an androgen-independent cancer cell type. It was found that compound 1 exhibited no significant cytotoxicity at concentrations below 50 μM to human PCa cells, including 22Rv1, C4-2, and PC-3, like normal cell HEK293T. In addition, we presented that 1 inhibited the invasiveness and proliferation of 22Rv1, PC-3, and C4-2 cells by suppressing the activation of p-AKT, p-mTOR, p-STAT3, HSP90, and HSP70. Moreover, treatment with 1 decreased the mRNA expression level of ErbB4, PDK1, STAT3, HSP70, and HSP90 in some PCa cells. Therefore, compound 1 may have therapeutic potential in PCa due to its role in suppressing cancer proliferation and metastasis.

Keywords:  AKT/mTOR; Marine natural product; Vibrio spp.; motility; proliferation; prostate cancer

DOI:  https://doi.org/10.4014/jmb.2502.02035
Cancer Prev Res (Phila). 2025 May 13.

Mitochondrial DNA copy number assessment is a potent predictor for prostate cancer in White but not Black Individuals.

Melanie K Flores, Jessica L Janes, Mirajul Islam, Junxiang Wan, Jiali Liu, Romonia R Reams, Li-Ming Su, Kelvin Yen, Hemal H Mehta, Allison Reagan, Lauren E Howard, Emily Wiggins, Adriana C Vidal, Stephen J Freedland, Pinchas Cohen.

Black individuals are disproportionately burdened by prostate cancer compared to White individuals. The mitochondrion is an untapped source for prostate cancer (PCa) biomarkers, and previous work has shown altered mitochondrial DNA (mtDNA) copy number is linked to mitochondrial dysfunction and tumorigenesis. We assess whether mtDNA copy number is altered in patients with and without PCa in a racially specific manner. Circulating cell-free mtDNA copy number from plasma and mtDNA copy number from white blood cells (WBCs) were measured in 199 patients undergoing biopsy (50/50 White cases/controls and 50/49 Black cases/controls). MtDNA copy number was determined via ddPCR. Logistic regressions tested associations between mtDNA and PCa by race. The area under the curve (AUC) was compared between covariate-only models and models with mtDNA. In both plasma and WBCs, mtDNA copy number was significantly increased in cases compared to controls in White patients, but not in Black patients. Interestingly, Black controls had higher mtDNA copy number levels than White controls. Multivariable analysis revealed significant associations of Plasma mtDNA and WBC mtDNA with PCa for White patients only. Elevated mtDNA copy number was more accurate in predicting PCa in White patients than in Black patients. Higher mtDNA copy number levels were associated with PCa in both Black and White patients. Plasma mtDNA may be more accurate than WBC mtDNA in predicting PCa incidence in Black men. Overall, Black controls had higher mtDNA copy number levels than White controls, suggesting mtDNA copy number may be implicated in PCa health disparities.

DOI: https://doi.org/10.1158/1940-6207.CAPR-24-0401