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Updated: Jan 16, 2026

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Genetics-Driven, Intensity-Modulated Adaptive Management of Patients With Metastatic Prostate Cancer.

Reynier D Rodriguez Rosales1, Arjun Venkatesh1, Jean-Pierre Kanumuambidi1

  • 1Department of Urology, University of Florida College of Medicine - Jacksonville, Jacksonville, Florida, USA.

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|October 5, 2025
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Summary
This summary is machine-generated.

Genomic alterations in specific gene clusters, mainly in lymph node-only metastatic prostate cancer (mPC), explain survival differences. These findings may guide intensified follow-up and novel combination therapies.

Keywords:
genetic alterationsmetastatic diseasenext‐generation sequencingprostate cancertumor tropism

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Area of Science:

  • Oncology
  • Genomics
  • Cancer Research

Background:

  • Survival outcomes for men with metastatic prostate cancer (mPC) significantly differ based on metastasis site (lymph nodes vs. bone).
  • Understanding the genomic basis for this disparity is crucial for personalized treatment and follow-up strategies.

Purpose of the Study:

  • To investigate whether site-specific genomic alterations and their combinations explain the survival gap in men with mPC.
  • To identify genomic signatures that could inform intensity-modulated follow-up or therapeutic interventions.

Main Methods:

  • Analysis of clinical and targeted-sequencing data from 1011 men with mPC using the cBioPortal registry.
  • Assessment of individual genes and multigene clusters for associations with overall survival (OS), identifying significant differences using Kaplan-Meier curves and dRMST.
  • Exploration of synthetic-lethal (SL) interactions using the SLOAD database.

Main Results:

  • 18 of 184 profiled genes (9.8%) showed significant alterations. Specific genes were enriched in either bone or lymph node metastases.
  • 65 multigene clusters were associated with inferior OS, predominantly in the lymph node-only mPC subgroup.
  • High-risk clusters predicted OS divergence 10-60 months post-metastasis diagnosis; 615 putative SL pairs were identified.

Conclusions:

  • Site-specific multigene clusters, particularly in lymph node mPC, underlie the survival disparity between nodal and bone metastases.
  • Identified genomic signatures suggest a 10-60 month window for intensity-modulated follow-up.
  • Hundreds of synthetic-lethal gene-alteration pairs offer potential for future combinatorial therapeutic strategies in mPC.