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  1. nature
  2. npj precision oncology
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  4. article
Genomic landscape and precision therapy in prostate cancer: current status and future directions
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  • Review
  • Open access
  • Published: 14 March 2026

Genomic landscape and precision therapy in prostate cancer: current status and future directions

  • John A. Ligon1,2,
  • Shashi Anand2,3,
  • Seema Singh2,3,
  • Jawed A. Siddiqui2,3,
  • John Clark Henegan2,4 &
  • …
  • Ajay Pratap Singh2,3 

npj Precision Oncology , Article number:  (2026) Cite this article

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We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Subjects

  • Cancer
  • Computational biology and bioinformatics
  • Oncology

Abstract

Prostate cancer continues to impose a significant health burden worldwide and in the United States, with rising incidence, persistent mortality rates, and disparities in both incidence and patient outcomes. Advances in genomic profiling have highlighted the remarkable heterogeneity of prostate cancer, revealing frequent alterations in key oncogenes, tumor suppressors, and pathways such as androgen receptor signaling and DNA damage repair that drive disease progression and therapy resistance. These molecular discoveries and their mechanistic validation in laboratory and preclinical models are transforming prostate cancer management, enabling more precise, biomarker-driven treatments and clinical trials. However, challenges, including intra- and inter-tumor genomic diversity, remain formidable barriers to progress. This review provides an overview of the current genomic landscape of prostate cancer and discusses recent advances in precision therapy. We also discuss emerging directions in integrating molecular profiling with personalized patient care, while addressing the roadblocks hampering progress. The discussion highlights the critical need for continued innovation in the development of personalized therapies to improve the clinical outcomes for patients with prostate cancer.

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Data availability

All publicly available information was used and analyzed to prepare this review.

References

  1. Kratzer, T. B. et al. Prostate cancer statistics, 2025. CA Cancer J Clin, 2025.

  2. Siegel, R. L. et al. Cancer statistics, 2025. CA Cancer J. Clin. 75, 10–45 (2025).

    Google Scholar 

  3. Wu, F., Zhang, H. & Hao, M. Interactions between key genes and pathways in prostate cancer progression and therapy resistance. Front. Oncol. 15, 1467540 (2025).

    Google Scholar 

  4. Poon, D. M. C. et al. Treatment of metastatic castration-resistant prostate cancer: review of current evidence and synthesis of expert opinions on radioligand therapy. Front. Oncol. 15, 1530580 (2025).

    Google Scholar 

  5. Kron, K. J. et al. TMPRSS2-ERG fusion co-opts master transcription factors and activates NOTCH signaling in primary prostate cancer. Nat. Genet. 49, 1336–1345 (2017).

    Google Scholar 

  6. Hagglof, C. et al. TMPRSS2-ERG expression predicts prostate cancer survival and associates with stromal biomarkers. PLoS One 9, e86824 (2014).

    Google Scholar 

  7. Xu, Z. et al. Nuclear receptor ERRalpha and transcription factor ERG form a reciprocal loop in the regulation of TMPRSS2:ERG fusion gene in prostate cancer. Oncogene 37, 6259–6274 (2018).

    Google Scholar 

  8. Tian, T. V. et al. Identification of novel TMPRSS2:ERG mechanisms in prostate cancer metastasis: involvement of MMP9 and PLXNA2. Oncogene 33, 2204–2214 (2014).

    Google Scholar 

  9. Shah, N. et al. ERG-mediated coregulator complex formation maintains androgen receptor signaling in prostate cancer. Cancer Res. 80, 4612–4619 (2020).

    Google Scholar 

  10. Mehra, R. et al. Comprehensive assessment of TMPRSS2 and ETS family gene aberrations in clinically localized prostate cancer. Mod. Pathol. 20, 538–544 (2007).

    Google Scholar 

  11. Kumar-Sinha, C., Tomlins, S. A. & Chinnaiyan, A. M. Recurrent gene fusions in prostate cancer. Nat. Rev. Cancer 8, 497–511 (2008).

    Google Scholar 

  12. Tomlins, S. A. et al. Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer. Science 310, 644–648 (2005).

    Google Scholar 

  13. Barbieri, C. E. et al. Exome sequencing identifies recurrent SPOP, FOXA1 and MED12 mutations in prostate cancer. Nat. Genet. 44, 685–689 (2012).

    Google Scholar 

  14. Hernandez-Llodra, S. et al. SPOP and CHD1 alterations in prostate cancer: Relationship with PTEN loss, tumor grade, perineural infiltration, and PSA recurrence. Prostate 81, 1267–1277 (2021).

    Google Scholar 

  15. Zhang, H., Jin, X. & Huang, H. Deregulation of SPOP in Cancer. Cancer Res. 83, 489–499 (2023).

    Google Scholar 

  16. Blattner, M. et al. SPOP Mutation Drives Prostate Tumorigenesis In Vivo through Coordinate Regulation of PI3K/mTOR and AR Signaling. Cancer Cell 31, 436–451 (2017).

    Google Scholar 

  17. Jin, H. J. et al. Cooperativity and equilibrium with FOXA1 define the androgen receptor transcriptional program. Nat. Commun. 5, 3972 (2014).

    Google Scholar 

  18. Tam, K. J. et al. Clinically-observed FOXA1 mutations upregulate SEMA3C through transcriptional derepression in prostate cancer. Sci. Rep. 14, 7082 (2024).

    Google Scholar 

  19. Peacock, J. W. et al. SEMA3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1. EMBO Mol. Med. 10, 219–238 (2018).

    Google Scholar 

  20. Hernandez-Llodra, S. et al. SPOP and FOXA1 mutations are associated with PSA recurrence in ERG wt tumors, and SPOP downregulation with ERG-rearranged prostate cancer. Prostate 79, 1156–1165 (2019).

    Google Scholar 

  21. Parolia, A. et al. Distinct structural classes of activating FOXA1 alterations in advanced prostate cancer. Nature 571, 413–418 (2019).

    Google Scholar 

  22. Maddah, M. M. et al. Evaluation of the Prognostic Role of TP53 Gene Mutations in Prostate Cancer Outcome: A Systematic Review and Meta-Analysis. Clin. Genitourin. Cancer 22, 102226 (2024).

    Google Scholar 

  23. Tan, H. L. et al. Rb loss is characteristic of prostatic small cell neuroendocrine carcinoma. Clin. Cancer Res. 20, 890–903 (2014).

    Google Scholar 

  24. Ku, S. Y. et al. Rb1 and Trp53 cooperate to suppress prostate cancer lineage plasticity, metastasis, and antiandrogen resistance. Science 355, 78–83 (2017).

    Google Scholar 

  25. Whang, Y. E. et al. Inactivation of the tumor suppressor PTEN/MMAC1 in advanced human prostate cancer through loss of expression. Proc. Natl. Acad. Sci. USA 95, 5246–5250 (1998).

    Google Scholar 

  26. Pungsrinont, T., Kallenbach, J. & Baniahmad, A. Role of PI3K-AKT-mTOR pathway as a pro-survival signaling and resistance-mediating mechanism to therapy of prostate cancer. Int. J. Mol. Sci. 22 (2021).

  27. Latini, J. M. et al. Loss of heterozygosity and microsatellite instability at chromosomal sites 1Q and 10Q in morphologically distinct regions of late stage prostate lesions. J. Urol. 166, 1931–1936 (2001).

    Google Scholar 

  28. Suzuki, H. et al. Interfocal heterogeneity of PTEN/MMAC1 gene alterations in multiple metastatic prostate cancer tissues. Cancer Res. 58, 204–209 (1998).

    Google Scholar 

  29. Antao, A. M., Ramakrishna, S. & Kim, K. S. The Role of Nkx3.1 in Cancers and Stemness. Int. J. Stem Cells 14, 168–179 (2021).

    Google Scholar 

  30. Pengju, Z. et al. NKX3.1 potentiates TNF-alpha/CHX-induced apoptosis of prostate cancer cells through increasing caspase-3 expression and its activity. Biochem. Biophys. Res. Commun. 398, 457–461 (2010).

    Google Scholar 

  31. Bowen, C., Zheng, T. & Gelmann, E. P. NKX3.1 Suppresses TMPRSS2-ERG Gene Rearrangement and Mediates Repair of Androgen Receptor-Induced DNA Damage. Cancer Res. 75, 2686–2698 (2015).

    Google Scholar 

  32. Sooreshjani, M. A. et al. LIMK2-NKX3.1 engagement promotes castration-resistant prostate cancer. Cancers 13, 2324 (2021).

  33. Huang, S. et al. Recurrent deletion of CHD1 in prostate cancer with relevance to cell invasiveness. Oncogene 31, 4164–4170 (2012).

    Google Scholar 

  34. Augello, M. A. et al. CHD1 Loss Alters AR binding at lineage-specific enhancers and modulates distinct transcriptional programs to drive prostate Tumorigenesis. Cancer Cell 35, 603–617 e8 (2019).

    Google Scholar 

  35. Kari, V. et al. Loss of CHD1 causes DNA repair defects and enhances prostate cancer therapeutic responsiveness. EMBO Rep. 17, 1609–1623 (2016).

    Google Scholar 

  36. Zhou, J. et al. Human CHD1 is required for early DNA-damage signaling and is uniquely regulated by its N terminus. Nucleic Acids Res. 46, 3891–3905 (2018).

    Google Scholar 

  37. Shenoy, T. R. et al. CHD1 loss sensitizes prostate cancer to DNA damaging therapy by promoting error-prone double-strand break repair. Ann. Oncol. 28, 1495–1507 (2017).

    Google Scholar 

  38. Blattner, M. et al. SPOP mutations in prostate cancer across demographically diverse patient cohorts. Neoplasia 16, 14–20 (2014).

    Google Scholar 

  39. Kaffenberger, S. D. & Barbieri, C. E. Molecular subtyping of prostate cancer. Curr. Opin. Urol. 26, 213–218 (2016).

    Google Scholar 

  40. Jenkins, R. B. et al. Detection of c-myc oncogene amplification and chromosomal anomalies in metastatic prostatic carcinoma by fluorescence in situ hybridization. Cancer Res. 57, 524–531 (1997).

    Google Scholar 

  41. Qiu, X. et al. MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets. Nat. Commun. 13, 2559 (2022).

    Google Scholar 

  42. Fromont, G. et al. 8q24 amplification is associated with Myc expression and prostate cancer progression and is an independent predictor of recurrence after radical prostatectomy. Hum. Pathol. 44, 1617–1623 (2013).

    Google Scholar 

  43. Bastacky, S. et al. Use of interphase fluorescence in situ hybridization in prostate needle biopsy specimens with isolated high-grade prostatic intraepithelial neoplasia as a predictor of prostate adenocarcinoma on follow-up biopsy. Hum. Pathol. 35, 281–289 (2004).

    Google Scholar 

  44. Jin, W. H. et al. The Molecular, Immunologic, and Clinicodemographic Landscape of MYC-Amplified Advanced Prostate Cancer. Clin. Genitourin. Cancer 22, e163–e169.e1 (2024).

    Google Scholar 

  45. Fujita, K. & Nonomura, N. Role of Androgen Receptor in Prostate Cancer: A Review. World J. Mens. Health 37, 288–295 (2019).

    Google Scholar 

  46. Quistini, A. et al. Androgen Receptor Signalling in Prostate Cancer: Mechanisms of Resistance to Endocrine Therapies. Res. Rep. Urol. 17, 211–223 (2025).

    Google Scholar 

  47. Azad, A. A. et al. Androgen Receptor Gene Aberrations in Circulating Cell-Free DNA: Biomarkers of Therapeutic Resistance in Castration-Resistant Prostate Cancer. Clin. Cancer Res. 21, 2315–2324 (2015).

    Google Scholar 

  48. Anand, S. et al. MYB and HIF1alpha crosstalk drives hypoxia-induced transcriptional reprogramming and adaptive signaling alterations in pancreatic cancer. Cancer Lett. 631, 217916 (2025).

    Google Scholar 

  49. Anand, S. et al. From modulation of cellular plasticity to potentiation of therapeutic resistance: new and emerging roles of MYB transcription factors in human malignancies. Cancer Metastas. Rev. 43, 409–421 (2024).

    Google Scholar 

  50. Edwards, J. et al. Gene amplifications associated with the development of hormone-resistant prostate cancer. Clin. Cancer Res. 9, 5271–5281 (2003).

    Google Scholar 

  51. Srivastava, S. K. et al. Myb overexpression overrides androgen depletion-induced cell cycle arrest and apoptosis in prostate cancer cells, and confers aggressive malignant traits: potential role in castration resistance. Carcinogenesis 33, 1149–1157 (2012).

    Google Scholar 

  52. Srivastava, S. K. et al. MYB interacts with androgen receptor, sustains its ligand-independent activation and promotes castration resistance in prostate cancer. Br. J. Cancer 126, 1205–1214 (2022).

    Google Scholar 

  53. Khan, M. A. et al. MYB exhibits racially disparate expression, clinicopathologic association, and predictive potential for biochemical recurrence in prostate cancer. iScience 26, 108487 (2023).

    Google Scholar 

  54. Lu, X. et al. An In Vivo Screen Identifies PYGO2 as a Driver for Metastatic Prostate Cancer. Cancer Res. 78, 3823–3833 (2018).

    Google Scholar 

  55. Andrews, P. G. & Kao, K. R. Wnt/beta-catenin-dependent acetylation of Pygo2 by CBP/p300 histone acetyltransferase family members. Biochem. J. 473, 4193–4203 (2016).

    Google Scholar 

  56. Ling, J. et al. Pygo2 activates BRPF1 via Pygo2-H3K4me2/3 interaction to maintain malignant progression in colon cancer. Exp. Cell Res. 431, 113696 (2023).

    Google Scholar 

  57. Andrews, P. G. P. et al. Augmentation of Myc-Dependent Mitotic Gene Expression by the Pygopus2 Chromatin Effector. Cell Rep. 23, 1516–1529 (2018).

    Google Scholar 

  58. Kao, K. R. et al. PYGOPUS2 expression in prostatic adenocarcinoma is a potential risk stratification marker for PSA progression following radical prostatectomy. J. Clin. Pathol. 71, 402–411 (2018).

    Google Scholar 

  59. Zhu, Y. et al. Targeting the chromatin effector Pygo2 promotes cytotoxic T cell responses and overcomes immunotherapy resistance in prostate cancer. Sci. Immunol. 8, eade4656 (2023).

    Google Scholar 

  60. Melling, N. et al. Overexpression of enhancer of zeste homolog 2 (EZH2) characterizes an aggressive subset of prostate cancers and predicts patient prognosis independently from pre- and postoperatively assessed clinicopathological parameters. Carcinogenesis 36, 1333–1340 (2015).

    Google Scholar 

  61. Henrique, R. & Jeronimo, C. Molecular detection of prostate cancer: a role for GSTP1 hypermethylation. Eur. Urol. 46, 660–669 (2004). discussion 669.

    Google Scholar 

  62. Mian, O. Y. et al. GSTP1 Loss results in accumulation of oxidative DNA base damage and promotes prostate cancer cell survival following exposure to protracted oxidative stress. Prostate 76, 199–206 (2016).

    Google Scholar 

  63. Kanwal, R. et al. Protection against oxidative DNA damage and stress in human prostate by glutathione S-transferase P1. Mol. Carcinog. 53, 8–18 (2014).

    Google Scholar 

  64. Kumar, B. & Lupold, S. E. MicroRNA expression and function in prostate cancer: a review of current knowledge and opportunities for discovery. Asian J. Androl. 18, 559–567 (2016).

    Google Scholar 

  65. Acharya, S. et al. Biphasic transcriptional and posttranscriptional regulation of MYB by androgen signaling mediates its growth control in prostate cancer. J. Biol. Chem. 299, 102725 (2023).

    Google Scholar 

  66. Holtrop, P., Swails, T. & Riggs, T. Hypertriglyceridemia in extremely low birth weight infants receiving lipid emulsions. J. Neonatal Perinat. Med. 8, 133–136 (2015).

    Google Scholar 

  67. Kumar, B. et al. Cell-type specific expression of oncogenic and tumor suppressive microRNAs in the human prostate and prostate cancer. Sci. Rep. 8, 7189 (2018).

    Google Scholar 

  68. Smith, B., Agarwal, P. & Bhowmick, N. A. MicroRNA applications for prostate, ovarian and breast cancer in the era of precision medicine. Endocr. Relat. Cancer 24, R157–R172 (2017).

    Google Scholar 

  69. Doldi, V. et al. Dissecting the role of microRNAs in prostate cancer metastasis: implications for the design of novel therapeutic approaches. Cell Mol. Life Sci. 73, 2531–2542 (2016).

    Google Scholar 

  70. Zenner, M. L. et al. Prostate-derived circulating microRNAs add prognostic value to prostate cancer risk calculators. J. Extracell. Biol. 2, e122 (2023).

  71. Rodarte, K. E. et al. Neuroendocrine Differentiation in Prostate Cancer Requires ASCL1. Cancer Res. 84, 3522–3537 (2024).

    Google Scholar 

  72. Russo, M. V. et al. SOX2 boosts major tumor progression genes in prostate cancer and is a functional biomarker of lymph node metastasis. Oncotarget 7, 12372–12385 (2016).

    Google Scholar 

  73. Wang, Z. et al. FOXA2 rewires AP-1 for transcriptional reprogramming and lineage plasticity in prostate cancer. Nat. Commun. 15, 4914 (2024).

    Google Scholar 

  74. Rotinen, M. et al. ONECUT2 is a targetable master regulator of lethal prostate cancer that suppresses the androgen axis. Nat. Med. 24, 1887–1898 (2018).

    Google Scholar 

  75. Bishop, J. L. et al. The Master Neural Transcription Factor BRN2 is an androgen receptor-suppressed driver of neuroendocrine differentiation in prostate cancer. Cancer Discov. 7, 54–71 (2017).

    Google Scholar 

  76. Imamura, J. et al. Lineage plasticity and treatment resistance in prostate cancer: the intersection of genetics, epigenetics, and evolution. Front. Endocrinol. 14, 1191311 (2023).

  77. Dardenne, E. et al. N-Myc Induces an EZH2-Mediated Transcriptional Program Driving Neuroendocrine Prostate Cancer. Cancer Cell 30, 563–577 (2016).

    Google Scholar 

  78. Liu, B. et al. PARP Inhibition Suppresses GR-MYCN-CDK5-RB1-E2F1 Signaling and Neuroendocrine Differentiation in Castration-Resistant Prostate Cancer. Clin. Cancer Res. 25, 6839–6851 (2019).

    Google Scholar 

  79. Maylin, Z. R. et al. Therapeutic exploitation of neuroendocrine transdifferentiation drivers in prostate cancer. Cells 13, 1999 (2024).

  80. Abida, W. et al. Analysis of the prevalence of microsatellite instability in prostate cancer and response to immune checkpoint blockade. JAMA Oncol. 5, 471–478 (2019).

    Google Scholar 

  81. Klumper, N. et al. The Role of Microsatellite Instability/DNA mismatch repair deficiency and tumor mutational burden as biomarkers in predicting response to immunotherapy in castration-resistant prostate cancer. Eur. Urol. 86, 388–390 (2024).

    Google Scholar 

  82. Lenis, A. T. et al. Microsatellite instability, tumor mutational burden, and response to immune checkpoint blockade in patients with prostate cancer. Clin. Cancer Res. 30, 3894–3903 (2024).

    Google Scholar 

  83. Mateo, J. et al. DNA-Repair Defects and Olaparib in Metastatic Prostate Cancer. N. Engl. J. Med. 373, 1697–1708 (2015).

    Google Scholar 

  84. Karlsson, Q. et al. Rare Germline Variants in ATM Predispose to Prostate Cancer: A PRACTICAL Consortium Study. Eur. Urol. Oncol. 4, 570–579 (2021).

    Google Scholar 

  85. Stolarova, L. et al. CHEK2 germline variants in cancer predisposition: stalemate rather than checkmate. Cells 9, 2675 (2020).

  86. Nyberg, T., Tischkowitz, M. & Antoniou, A. C. BRCA1 and BRCA2 pathogenic variants and prostate cancer risk: systematic review and meta-analysis. Br. J. Cancer 126, 1067–1081 (2022).

    Google Scholar 

  87. Ledet, E. M. et al. Comparison of germline mutations in African American and Caucasian men with metastatic prostate cancer. Prostate 81, 433–439 (2021).

    Google Scholar 

  88. Nyberg, T. et al. Prostate Cancer Risks for Male BRCA1 and BRCA2 Mutation Carriers: A Prospective Cohort Study. Eur. Urol. 77, 24–35 (2020).

    Google Scholar 

  89. Agalliu, I. et al. Associations of high-grade prostate cancer with BRCA1 and BRCA2 founder mutations. Clin. Cancer Res. 15, 1112–1120 (2009).

    Google Scholar 

  90. Oh, M. et al. The association of BRCA1 and BRCA2 mutations with prostate cancer risk, frequency, and mortality: A meta-analysis. Prostate 79, 880–895 (2019).

    Google Scholar 

  91. Nyberg, T. et al. Homeobox B13 G84E Mutation and Prostate Cancer Risk. Eur. Urol. 75, 834–845 (2019).

    Google Scholar 

  92. Ewing, C. M. et al. Germline mutations in HOXB13 and prostate-cancer risk. N. Engl. J. Med. 366, 141–149 (2012).

    Google Scholar 

  93. Karlsson, R. et al. A population-based assessment of germline HOXB13 G84E mutation and prostate cancer risk. Eur. Urol. 65, 169–176 (2014).

    Google Scholar 

  94. Darst, B. F. et al. Germline Sequencing DNA Repair Genes in 5545 Men With Aggressive and Nonaggressive Prostate Cancer. J. Natl. Cancer Inst. 113, 616–625 (2021).

    Google Scholar 

  95. Zhang, X. et al. ATM-AMPKalpha mediated LAG-3 expression suppresses T cell function in prostate cancer. Cell Immunol. 393-394, 104773 (2023).

    Google Scholar 

  96. Wu, Y. et al. A comprehensive evaluation of CHEK2 germline mutations in men with prostate cancer. Prostate 78, 607–615 (2018).

    Google Scholar 

  97. Cybulski, C. et al. A novel founder CHEK2 mutation is associated with increased prostate cancer risk. Cancer Res. 64, 2677–2679 (2004).

    Google Scholar 

  98. Pritchard, C. C. et al. Inherited DNA-Repair Gene Mutations in Men with Metastatic Prostate Cancer. N. Engl. J. Med. 375, 443–453 (2016).

    Google Scholar 

  99. Heijink, A. M. et al. BRCA2 deficiency instigates cGAS-mediated inflammatory signaling and confers sensitivity to tumor necrosis factor-alpha-mediated cytotoxicity. Nat. Commun. 10, 100 (2019).

    Google Scholar 

  100. Hu, M. et al. ATM inhibition enhances cancer immunotherapy by promoting mtDNA leakage and cGAS/STING activation. J. Clin. Invest. 131, e139333 (2021).

  101. Zhao, D. et al. Chromatin Regulator CHD1 Remodels the Immunosuppressive Tumor Microenvironment in PTEN-Deficient Prostate Cancer. Cancer Discov. 10, 1374–1387 (2020).

    Google Scholar 

  102. Vidotto, T. et al. PTEN-deficient prostate cancer is associated with an immunosuppressive tumor microenvironment mediated by increased expression of IDO1 and infiltrating FoxP3+ T regulatory cells. Prostate 79, 969–979 (2019).

    Google Scholar 

  103. Graham, M. K. et al. Convergent alterations in the tumor microenvironment of MYC-driven human and murine prostate cancer. Nat. Commun. 15, 7414 (2024).

    Google Scholar 

  104. Casey, S. C. et al. MYC regulates the antitumor immune response through CD47 and PD-L1. Science 352, 227–231 (2016).

    Google Scholar 

  105. Chesner, L. N. et al. Androgen Receptor Inhibition Increases MHC Class I Expression and Improves Immune Response in Prostate Cancer. Cancer Discov. 15, 481–494 (2025).

    Google Scholar 

  106. Wang, D. et al. IL-1beta Is an Androgen-Responsive Target in Macrophages for Immunotherapy of Prostate Cancer. Adv. Sci. 10, e2206889 (2023).

    Google Scholar 

  107. Hu, Y. M. et al. Elevated Tumor-Associated Androgen Receptor Activity Correlates with Poor Immune Infiltration and Immunotherapy Response across Cancer Types. Cancer Res Commun. 6, 17–35 (2026).

    Google Scholar 

  108. Bhinder, B. et al. Immunogenomic Landscape of Neuroendocrine Prostate Cancer. Clin. Cancer Res 29, 2933–2943 (2023).

    Google Scholar 

  109. Li, S. et al. Defined cellular reprogramming of androgen receptor-active prostate cancer to neuroendocrine prostate cancer. bioRxivp, (2025).

  110. Zennami, K. et al. PDCD4 Is an androgen-repressed tumor suppressor that regulates prostate cancer growth and castration resistance. Mol. Cancer Res. 17, 618–627 (2019).

    Google Scholar 

  111. Xi, J. et al. miR-21 depletion in macrophages promotes tumoricidal polarization and enhances PD-1 immunotherapy. Oncogene 37, 3151–3165 (2018).

    Google Scholar 

  112. Sun, T. et al. MiR-221 promotes the development of androgen independence in prostate cancer cells via downregulation of HECTD2 and RAB1A. Oncogene 33, 2790–2800 (2014).

    Google Scholar 

  113. Tan, S. et al. Exosomal miRNAs in tumor microenvironment. J. Exp. Clin. Cancer Res. 39, 67 (2020).

    Google Scholar 

  114. Yu, E. Y. et al. Germline and Somatic Genomic Testing for Metastatic Prostate Cancer: ASCO Guideline. J. Clin. Oncol. 43, 748–758 (2025).

    Google Scholar 

  115. Antonarakis, E. S. et al. AR-V7 and resistance to enzalutamide and abiraterone in prostate cancer. N. Engl. J. Med. 371, 1028–1038 (2014).

    Google Scholar 

  116. Scher, H. I. et al. Association of AR-V7 on circulating tumor cells as a treatment-specific biomarker with outcomes and survival in castration-resistant prostate cancer. JAMA Oncol. 2, 1441–1449 (2016).

    Google Scholar 

  117. Zhang, T. et al. Androgen Receptor Splice Variant, AR-V7, as a Biomarker of Resistance to Androgen Axis-Targeted Therapies in Advanced Prostate Cancer. Clin. Genitourin. Cancer 18, 1–10 (2020).

    Google Scholar 

  118. Hille, C. et al. Detection of Androgen Receptor Variant 7 (ARV7) mRNA Levels in EpCAM-Enriched CTC Fractions for Monitoring Response to Androgen Targeting Therapies in Prostate Cancer. Cells. 8, 1067 (2019).

  119. Nyquist, M. D. et al. Combined TP53 and RB1 loss promotes prostate cancer resistance to a spectrum of therapeutics and confers vulnerability to replication stress. Cell Rep. 31, 107669 (2020).

    Google Scholar 

  120. Jamaspishvili, T. et al. Clinical implications of PTEN loss in prostate cancer. Nat. Rev. Urol. 15, 222–234 (2018).

    Google Scholar 

  121. Yoshida, S. et al. TAS3681, an androgen receptor antagonist, prevents drug resistance driven by aberrant androgen receptor signaling in prostate cancer. Mol. Oncol. 18, 1980–2000 (2024).

    Google Scholar 

  122. Bourlon, M. T., Valdez, P. & Castro, E. Development of PARP inhibitors in advanced prostate cancer. Ther. Adv. Med. Oncol. 16, 17588359231221337 (2024).

    Google Scholar 

  123. de Bono, J. et al. Olaparib for Metastatic Castration-Resistant Prostate Cancer. N. Engl. J. Med. 382, 2091–2102 (2020).

    Google Scholar 

  124. Abida, W. et al. Rucaparib for the Treatment of Metastatic Castration-resistant Prostate Cancer Associated with a DNA Damage Repair Gene Alteration: Final Results from the Phase 2 TRITON2 Study. Eur. Urol. 84, 321–330 (2023).

    Google Scholar 

  125. Clarke, N. W. et al. Abiraterone and Olaparib for Metastatic Castration-Resistant Prostate Cancer. NEJM Evid. 1, EVIDoa2200043 (2022).

    Google Scholar 

  126. Agarwal, N. et al. Talazoparib plus enzalutamide in men with metastatic castration-resistant prostate cancer: final overall survival results from the randomised, placebo-controlled, phase 3 TALAPRO-2 trial. Lancet 406, 447–460 (2025).

    Google Scholar 

  127. Hussain, M. et al. Abiraterone, Olaparib, or Abiraterone + Olaparib in First-Line Metastatic Castration-Resistant Prostate Cancer with DNA Repair Defects (BRCAAway). Clin. Cancer Res. 30, 4318–4328 (2024).

    Google Scholar 

  128. Attard, G. et al. Niraparib and abiraterone acetate plus prednisone for HRR-deficient metastatic castration-sensitive prostate cancer: a randomized phase 3 trial. Nat. Med. 31, 4109–4118 (2025).

  129. Fizazi, K. et al. Capivasertib plus abiraterone in PTEN-deficient metastatic hormone-sensitive prostate cancer: CAPItello-281 Phase III study. Ann. Oncol. 37, 53–68 (2026).

  130. Rescigno, P. et al. Capivasertib in combination with enzalutamide for metastatic castration resistant prostate cancer after docetaxel and abiraterone: Results from the randomized phase II RE-AKT trial. Eur. J. Cancer 205, 114103 (2024).

    Google Scholar 

  131. Crabb, S. J. et al. Pan-AKT Inhibitor Capivasertib With Docetaxel and Prednisolone in Metastatic Castration-Resistant Prostate Cancer: A Randomized, Placebo-Controlled Phase II Trial (ProCAID). J. Clin. Oncol. 39, 190–201 (2021).

    Google Scholar 

  132. AstraZeneca, TRUQAP® (capivasertib) combination in PTEN-deficient metastatic hormone-sensitive prostate cancer demonstrated statistically significant and clinically meaningful improvement in radiographic progression-free survival in CAPItello-281 Phase III trial. AstraZeneca Media. (2024).

  133. Sweeney, C. et al. Ipatasertib plus abiraterone and prednisolone in metastatic castration-resistant prostate cancer (IPATential150): a multicentre, randomised, double-blind, phase 3 trial. Lancet 398, 131–142 (2021).

    Google Scholar 

  134. de Bono, J. S. et al. Final Overall Survival and Molecular Data Associated with Clinical Outcomes in Patients Receiving Ipatasertib and Abiraterone in the Phase 3 IPATential150 Trial. Eur. Urol. 87, 672–682 (2025).

    Google Scholar 

  135. Michael Thomas Schweizer, K.P., Atish Dipankar Choudhury, Emiliano Calvo, Richard C. Frank, Li Liu, Rajendar K. Mittapalli, Jessica Tougias, Claudia Andreu-Vieyra, Timothy Geoffrey Bowler, Neelesh Soman, and Benjamin Garmezy, Phase 1 trial of mevrometostat (PF-06821497), a potent and selective inhibitor of enhancer of zeste homolog 2 (EZH2), in castration-resistant prostate cancer (CRPC). in 2024 ASCO Annual MeetingJ. Clin. Oncol. (2024).

  136. Aggarwal, R. et al. Safety and Efficacy of Tarlatamab in Patients with Neuroendocrine Prostate Cancer: Results from the Phase 1b DeLLpro-300 Study. Clin. Cancer Res. 31, 3854–3863 (2025).

    Google Scholar 

  137. Dorff, T. B. et al. PSCA-CAR T cell therapy in metastatic castration-resistant prostate cancer: a phase 1 trial. Nat. Med. 30, 1636–1644 (2024).

    Google Scholar 

  138. Narayan, V. et al. PSMA-targeting TGFbeta-insensitive armored CAR T cells in metastatic castration-resistant prostate cancer: a phase 1 trial. Nat. Med. 28, 724–734 (2022).

    Google Scholar 

  139. Le, D. T. et al. Pembrolizumab for previously treated, microsatellite instability-high/mismatch repair-deficient advanced colorectal cancer: final analysis of KEYNOTE-164. Eur. J. Cancer 186, 185–195 (2023).

    Google Scholar 

  140. Graham, L. S. et al. Mismatch repair deficiency in metastatic prostate cancer: Response to PD-1 blockade and standard therapies. PLoS One 15, e0233260 (2020).

    Google Scholar 

  141. Wu, Y. M. et al. Inactivation of CDK12 Delineates a Distinct Immunogenic Class of Advanced Prostate Cancer. Cell 173, 1770–1782.e14 (2018).

    Google Scholar 

  142. Higa, K. et al. Efficacy of pembrolizumab in MSI-high and BRCA-positive castration-resistant prostate cancer. Cancer Genet. 296-297, 41–44 (2025).

    Google Scholar 

  143. Peyraud, F. & Italiano, A. Combined PARP inhibition and immune checkpoint therapy in solid tumors. Cancers 12, 1502 (2020).

  144. Rescigno, P. et al. PERSEUS1: An Open-label, Investigator-initiated, Single arm, Phase 2 Trial Testing the Efficacy of Pembrolizumab in Patients with Metastatic Castration-resistant Prostate Cancer with Mismatch Repair Deficiency and Other Immune-sensitive Molecular Subtypes. Eur. Urol. Oncol. 8, 1059–1069 (2025).

    Google Scholar 

  145. Sharma, P. et al. Nivolumab Plus Ipilimumab for Metastatic Castration-Resistant Prostate Cancer: Preliminary Analysis of Patients in the CheckMate 650 Trial. Cancer Cell 38, 489–499.e3 (2020).

    Google Scholar 

  146. Leone, G. et al. Nivolumab and Ipilimumab for Metastatic Castration-Resistant Prostate Cancer With an Immunogenic Signature: The Multicenter, Two-Cohort, Phase II NEPTUNES Study. J. Clin. Oncol. 43, 3070–3080 (2025).

    Google Scholar 

  147. You, G. et al. B7-H3x4-1BB bispecific antibody augments antitumor immunity by enhancing terminally differentiated CD8(+) tumor-infiltrating lymphocytes. Sci. Adv. 7, eaax3160 (2021).

  148. Aggarwal, C. et al. Dual checkpoint targeting of B7-H3 and PD-1 with enoblituzumab and pembrolizumab in advanced solid tumors: interim results from a multicenter phase I/II trial. J. Immunother. Cancer 10, e004424 (2022).

  149. Shi, W. et al. Immune checkpoint B7-H3 is a therapeutic vulnerability in prostate cancer harboring PTEN and TP53 deficiencies. Sci. Transl. Med. 15, eadf6724 (2023).

    Google Scholar 

  150. Sartor, O. et al. Lutetium-177-PSMA-617 for Metastatic Castration-Resistant Prostate Cancer. N. Engl. J. Med. 385, 1091–1103 (2021).

    Google Scholar 

  151. Fallah, J. et al. FDA Approval Summary: Lutetium Lu 177 Vipivotide Tetraxetan for Patients with Metastatic Castration-Resistant Prostate Cancer. Clin. Cancer Res 29, 1651–1657 (2023).

    Google Scholar 

  152. Boixareu, C. et al. Targeting the tumour cell surface in advanced prostate cancer. Nat. Rev. Urol. 22, 569–589 (2025).

    Google Scholar 

  153. Chen, B. et al. Antibody-drug conjugates in cancer therapy: current landscape, challenges, and future directions. Mol. Cancer 24, 279 (2025).

    Google Scholar 

  154. Giugliano, F. et al. Bystander effect of antibody-drug conjugates: fact or fiction? Curr. Oncol. Rep. 24, 809–817 (2022).

    Google Scholar 

  155. Petrylak, D. P. et al. Phase 1 study of PSMA ADC, an antibody-drug conjugate targeting prostate-specific membrane antigen, in chemotherapy-refractory prostate cancer. Prostate 79, 604–613 (2019).

    Google Scholar 

  156. Petrylak, D. P. et al. PSMA ADC monotherapy in patients with progressive metastatic castration-resistant prostate cancer following abiraterone and/or enzalutamide: Efficacy and safety in open-label single-arm phase 2 study. Prostate 80, 99–108 (2020).

    Google Scholar 

  157. Carrasquillo, J. A. et al. Imaging Patients with Metastatic Castration-Resistant Prostate Cancer Using (89)Zr-DFO-MSTP2109A Anti-STEAP1 Antibody. J. Nucl. Med 60, 1517–1523 (2019).

    Google Scholar 

  158. Danila, D. C. et al. Phase I Study of DSTP3086S, an Antibody-Drug Conjugate Targeting Six-Transmembrane Epithelial Antigen of Prostate 1, in Metastatic Castration-Resistant Prostate Cancer. J. Clin. Oncol. 37, 3518–3527 (2019).

    Google Scholar 

  159. Bardia, A. et al. Sacituzumab govitecan, a Trop-2-directed antibody-drug conjugate, for patients with epithelial cancer: final safety and efficacy results from the phase I/II IMMU-132-01 basket trial. Ann. Oncol. 32, 746–756 (2021).

    Google Scholar 

  160. Sardinha, M. et al. Antibody-Drug Conjugates in Prostate Cancer: A Systematic Review. Cureus 15, e34490 (2023).

    Google Scholar 

  161. Doi, T. et al. 453O DS-7300 (B7-H3 DXd antibody-drug conjugate [ADC]) shows durable antitumor activity in advanced solid tumors: Extended follow-up of a phase I/II study. Ann. Oncol. 33, S744–S745 (2022).

    Google Scholar 

  162. de Bono, J. S. et al. 1654P TAMARACK: Randomized Phase II trial of the B7-H3 targeting antibody drug conjugate (ADC) vobramitamab duocarmazine (vobra duo) in metastatic castration-resistant prostate cancer (mCRPC). Ann. Oncol. 35, S996–S997 (2024).

    Google Scholar 

  163. Corn, P. G. et al. Cabazitaxel plus carboplatin for the treatment of men with metastatic castration-resistant prostate cancers: a randomised, open-label, phase 1-2 trial. Lancet Oncol. 20, 1432–1443 (2019).

    Google Scholar 

  164. Li, H. et al. PARP inhibitor resistance: the underlying mechanisms and clinical implications. Mol. Cancer 19, 107 (2020).

    Google Scholar 

  165. Lin, K. K. et al. BRCA Reversion Mutations in Circulating Tumor DNA Predict Primary and Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma. Cancer Discov. 9, 210–219 (2019).

    Google Scholar 

  166. Hofstad, M. et al. Dual inhibition of ATR and DNA-PKcs radiosensitizes ATM-mutant prostate cancer. Oncogene 44, 1746–1760 (2025).

    Google Scholar 

  167. Rafiei, S. et al. ATM Loss Confers Greater Sensitivity to ATR Inhibition Than PARP Inhibition in Prostate Cancer. Cancer Res. 80, 2094–2100 (2020).

    Google Scholar 

  168. Fatteh, M. et al. Poly (ADP-ribose) Polymerase Inhibitor Resistance Driven by Emergence of Polyclonal Mutations With Convergent Evolution: A Molecular Tumor Board Discussion. JCO Precis. Oncol. 8, e2400254 (2024).

    Google Scholar 

  169. Harvey-Jones, E. et al. Longitudinal profiling identifies co-occurring BRCA1/2 reversions, TP53BP1, RIF1 and PAXIP1 mutations in PARP inhibitor-resistant advanced breast cancer. Ann. Oncol. 35, 364–380 (2024).

    Google Scholar 

  170. Derlin, T. et al. PSMA-heterogeneity in metastatic castration-resistant prostate cancer: Circulating tumor cells, metastatic tumor burden, and response to targeted radioligand therapy. Prostate 83, 1076–1088 (2023).

    Google Scholar 

  171. Current, K. et al. Investigating PSMA-Targeted Radioligand Therapy Efficacy as a Function of Cellular PSMA Levels and Intratumoral PSMA Heterogeneity. Clin. Cancer Res. 26, 2946–2955 (2020).

    Google Scholar 

  172. Bakht, M. K. & Beltran, H. Biological determinants of PSMA expression, regulation and heterogeneity in prostate cancer. Nat. Rev. Urol. 22, 26–45 (2025).

    Google Scholar 

  173. Beltran, H. et al. The Role of Lineage Plasticity in Prostate Cancer Therapy Resistance. Clin. Cancer Res 25, 6916–6924 (2019).

    Google Scholar 

  174. Thang, S. P. et al. Poor Outcomes for Patients with Metastatic Castration-resistant Prostate Cancer with Low Prostate-specific Membrane Antigen (PSMA) Expression Deemed Ineligible for (177)Lu-labelled PSMA Radioligand Therapy. Eur. Urol. Oncol. 2, 670–676 (2019).

    Google Scholar 

  175. Beshiri, M. et al. Prostate organoids: emerging experimental tools for translational research. J. Clin. Invest.133, e169616 (2023).

  176. Wong, E. Y., Chu, T. N. & Ladi-Seyedian, S. S. Genomics and Artificial Intelligence: Prostate Cancer. Urol. Clin. North Am. 51, 27–33 (2024).

    Google Scholar 

  177. Yan, L., Su, P. & Sun, X. Role of multi‑omics in advancing the understanding and treatment of prostate cancer (Review). Mol. Med. Rep. 31, 130 (2025).

  178. Yu, X. et al. Single-cell omics traces the heterogeneity of prostate cancer cells and the tumor microenvironment. Cell Mol. Biol. Lett. 28, 38 (2023).

    Google Scholar 

  179. Mei, S. et al. Single-cell and spatial transcriptomics reveal a tumor-associated macrophage subpopulation that mediates prostate cancer progression and metastasis. Mol. Cancer Res. 23, 653–665 (2025).

    Google Scholar 

  180. Figiel, S. et al. Spatial transcriptomic analysis of virtual prostate biopsy reveals confounding effect of tissue heterogeneity on genomic signatures. Mol. Cancer 22, 162 (2023).

    Google Scholar 

  181. Casanova-Salas, I. et al. Quantitative and qualitative analysis of blood-based liquid biopsies to inform clinical decision-making in prostate cancer. Eur. Urol. 79, 762–771 (2021).

    Google Scholar 

  182. Zhang, X. et al. Genetic and epigenetic features of neuroendocrine prostate cancer and their emerging applications. Int Rev. Cell Mol. Biol. 383, 41–66 (2024).

    Google Scholar 

  183. Bevere, M. et al. An overview of circulating biomarkers in neuroendocrine neoplasms: a clinical guide. Diagnostics 13, 2820 (2023).

  184. Zhao, S. G. et al. A clinical-grade liquid biomarker detects neuroendocrine differentiation in prostate cancer. J. Clin. Invest. 132, e161858 (2022).

  185. Crocetto, F. et al. Liquid biopsy in prostate cancer management-current challenges and future perspectives. Cancers 14, 3272 (2022).

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Acknowledgements

All figures in this manuscript were created with BioRender.com. We thank fellow clinicians, researchers, and all other members of the GU Cancer Working Group at the UMMC CCRI for their insightful discussion on the components presented in this manuscript. We would also like to acknowledge the funding support from the Department of Defense (HT9425-23-1-0452; W81XWH-22-1-0913) and the Cancer Center and Research Institute.

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Authors and Affiliations

  1. School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA

    John A. Ligon

  2. Cancer Center and Research Institute, University of Mississippi Medical Center, Jackson, MS, USA

    John A. Ligon, Shashi Anand, Seema Singh, Jawed A. Siddiqui, John Clark Henegan & Ajay Pratap Singh

  3. Department of Cell and Molecular Biology, School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA

    Shashi Anand, Seema Singh, Jawed A. Siddiqui & Ajay Pratap Singh

  4. Department of Medicine, School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA

    John Clark Henegan

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Contributions

Ajay P. Singh and John C. Henegan conceived and designed the manuscript. John A. Ligon conducted the literature review, performed data analysis, and prepared the first draft. Shashi Anand, Seema Singh, Jawed Siddiqui, John C. Henegan, and Ajay P. Singh reviewed the draft and suggested revisions, including the addition of relevant literature. Shashi Anand and Seema Singh contributed to the graphic design. John A. Ligon and Shashi Anand prepared the final revised version of the manuscript. All authors reviewed and approved the final manuscript for submission.

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Ligon, J.A., Anand, S., Singh, S. et al. Genomic landscape and precision therapy in prostate cancer: current status and future directions. npj Precis. Onc. (2026). https://doi.org/10.1038/s41698-026-01368-3

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  • Received: 20 November 2025

  • Accepted: 28 February 2026

  • Published: 14 March 2026

  • DOI: https://doi.org/10.1038/s41698-026-01368-3

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