Prognostic value of PARP1 and PARP2 copy number alterations in prostate cancer

PARP1/2 have overlapping yet nonredundant biological functions in DNA repair and androgen receptor-transcriptional regulation. Studies on PARP alterations in human tumors have yielded conflicting results. In prostate cancer (PCa), PARP1/2 protein overexpression has been related to androgen deprivati...

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Detalles Bibliográficos
Autores: Segalés Tañà, Laura, 1994-, Bellmunt Molins, Joaquim, 1959-, Perera Bel, Júlia, Vargas-Parra, Gardenia, Juanpere, Nuria, Lopez-Segura, David, Rodriguez-Vida, Alejo, Colomo Saperas, Luis Alberto, Cecchini Rosell, Lluís, Lloreta, Josep, 1958-, Yélamos López, José, Fumadó Ciutat, Lluis, Hernández Llodrà, Silvia
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2025
País:España
Institución:Universitat Pompeu Fabra
Repositorio:Repositorio Digital de la UPF
OAI Identifier:oai:repositori.upf.edu:10230/71940
Acceso en línea:http://hdl.handle.net/10230/71940
http://dx.doi.org/10.1016/j.labinv.2025.104171
Access Level:acceso embargado
Palabra clave:PARP inhibitors
PARP1
PARP2
Copy number
Prostate cancer
Descripción
Sumario:PARP1/2 have overlapping yet nonredundant biological functions in DNA repair and androgen receptor-transcriptional regulation. Studies on PARP alterations in human tumors have yielded conflicting results. In prostate cancer (PCa), PARP1/2 protein overexpression has been related to androgen deprivation therapy resistance, biochemical recurrence, and progression to metastases. PARP inhibitors have been approved for treating metastatic castration-resistant PCa with homologous recombination repair gene mutations. However, the significance of PARP1/2 genomic alterations is not fully studied. We aimed to analyze PARP1/2 alterations in PCa, assess their value as prognostic markers, and explore their relevance for potential therapeutic stratification. PARP1/2 copy number status was evaluated in 121 PCa primary tumors using real-time PCR. In 29 of them, a regional pelvic lymph node involvement was also analyzed. BRCA1/2 somatic mutations were analyzed in 24 PCa cases. Relationship with clinicopathological features, progression to metastases, and prostate-specific antigen recurrence was assessed. PARP1 loss and PARP2 gain were detected in 34.7% and 32.2% of primary tumors, respectively, with a high frequency of co-occurrence (P < .001). Both alterations were statistically associated with locally advanced disease at the time of diagnosis (P = .036; P = .006), metastatic dissemination (P = .014; P = .003), and other aggressive clinicopathological characteristics (such as the presence of Gleason pattern 5, high-grade, and high-stage). Cases with exclusive PARP2 gain had the shortest time to prostate-specific antigen recurrence, whereas double wt patients displayed the best outcome (P = .007). In 29 paired primary tumors and regional pelvic lymph node involvement, PARP1 loss showed strong concordance (P = .001), whereas PARP2 gain did not (P = .411). In conclusion, loss of PARP1 and gain of PARP2 show strong co-occurrence and are associated with clinicopathological characteristics of aggressiveness. PARP2 alterations appear to have a particularly significant impact on disease prognosis. Furthermore, these data suggest that the analysis of PARP1/2 copy number status could be useful in predicting PCa outcomes. Its role in therapy warrants further evaluation.