Molecular biology of prostate cancer
Perfilamiento molecular avanzado en sarcomas: claves para la práctica oncológica moderna
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Introduction: prostate cancer (PCa) is the most common malignant neoplasm in men and a significant cause of cancer-related deaths. Its heterogeneity, ranging from indolent to aggressive forms, complicates risk stratification and therapeutic selection. However, advances in molecular biology have clarified the genomic and epigenetic alterations involved in tumorigenesis, progression, and resistance, thereby driving the development of precision medicine.
Methods: a narrative literature review was conducted on the key molecular pathways, clinically relevant genomic alterations, and emerging biomarker-based therapeutic strategies for localized and metastatic PCa.
Results: germline and somatic mutations in DNA repair genes, such as BRCA1, BRCA2, and ATM, are associated with increased susceptibility, aggressive phenotypes, and sensitivity to PARP inhibitors and platinum-based regimens. Loss of tumor suppressor genes (PTEN, TP53, and RB1) promotes genomic instability, castration resistance, and unfavorable prognosis. Genomic classifiers (Oncotype DX, Decipher) refine risk stratification and guide therapeutic intensification or de-escalation in localized disease, whereas reflex genetic testing and biomarker-driven clinical trials exemplify the clinical integration of molecular data. In advanced disease, therapies targeting androgen receptors, DNA repair mechanisms, and PSMA are transforming PCa management.
Conclusions: molecular characterization of PCa enables biomarker-guided interventions that optimize therapeutic decisions and clinical outcomes. The systematic incorporation of genomic profiling is essential for consolidating precision medicine in treatment strategies.
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