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Molecular Pathology of Prostate Cancer

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Molecular Surgical Pathology

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Abstract

Adenocarcinoma of the prostate is the most common noncutaneous cancer and the second leading cause of cancer-related death in males in Western populations. Also, its incidence has been increasing in regions traditionally found to have much lower levels (e.g., those in East and South East Asia). Our understanding of the molecular alterations driving the initiation, progression, response to therapeutic interventions, and treatment resistance have accelerated rapidly in the last several years. Most prostate cancers, from initiation to castration-resistant metastatic disease, show overexpression of MYC as a key oncogenic driver. Recent work has provided insights into distinct molecular subtypes of prostate cancer characterized by ETS gene rearrangements (TMPRSS2-ERG being the most common) and somatic mutations in SPOP, FOXA1 and a number of epigenetic regulators. Recurrent somatic genomic aberrations include copy number changes and mutations in tumor suppressors (e.g., PTEN, TP53, NKX3.1, CDKN1B, RB1, BRCA2, and ATM) and oncogenes (e.g., MYC, AR), as well as numerous DNA methylation changes (e.g., GSTP1, PTGS2, APC, ENDRB, and RASSF1). Germline studies have uncovered inherited variants associated with prostate cancer including in HOXB13, several in chromosome 8q24 that are associated with the control of MYC expression, and a number of DNA repair genes involved in homologous recombination mediated repair (e.g., BRCA2 and ATM). Overall, approximately 20–25% of fatal, metastatic castration-resistant prostate cancers harbor either germline, somatic, or combined germline/somatic alterations in DNA repair genes involving either homologous recombination pathway genes or mismatch repair genes. A number of morphological variants of prostate cancer, including small cell neuroendocrine carcinoma and other “androgen receptor indifferent” lesions, occur infrequently in primary tumors. However, as an apparent resistance mechanism, in response to newer androgen ablation and AR targeting agents, their incidence may be rising. Current and future directions to further improve our understanding and treatment of this disease include the use of computational pathology/artificial intelligence, studies of the tumor microenvironment, and improved understanding of the roles of the prostate infection in disease initiation, progression, and response to treatment.

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  1. Departments of Pathology, Urology and Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, Baltimore, MD, USA

    Jiayu Chen, William G. Nelson, Karen Sfanos, Srinivasan Yegnasubramanian & Angelo M. De Marzo

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  1. Jiayu Chen
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  2. William G. Nelson
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  4. Srinivasan Yegnasubramanian
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  5. Angelo M. De Marzo
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Correspondence to Angelo M. De Marzo .

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  1. Department of Pathology and Laboratory Medicine, Indiana University Hospital, Indianapolis, IN, USA

    Liang Cheng

  2. Department of Pathology and Laboratory Medicine, University of Alabama at Birmingham, Birmingham, AL, USA

    George J. Netto

  3. Department of Pathology, Indiana University Hospital, Indianapolis, IN, USA

    John N. Eble

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Chen, J., Nelson, W.G., Sfanos, K., Yegnasubramanian, S., De Marzo, A.M. (2023). Molecular Pathology of Prostate Cancer. In: Cheng, L., Netto, G.J., Eble, J.N. (eds) Molecular Surgical Pathology. Springer, Cham. https://doi.org/10.1007/978-3-031-35118-1_14

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