Circulating tumour DNA reveals genetic traits of patients with intraductal carcinoma of the prostate.


Journal

BJU international
ISSN: 1464-410X
Titre abrégé: BJU Int
Pays: England
ID NLM: 100886721

Informations de publication

Date de publication:
03 2022
Historique:
revised: 05 06 2021
received: 20 02 2021
accepted: 22 06 2021
pubmed: 30 6 2021
medline: 16 4 2022
entrez: 29 6 2021
Statut: ppublish

Résumé

To investigate the genetic alterations of patients with prostate cancer (PCa) with and without intraductal carcinoma of the prostate (IDC-P). We performed targeted sequencing of plasma cell-free DNA on 161 patients with prostate adenocarcinoma (PAC) with IDC-P and 84 without IDC-P. Genomic alterations were compared between these two groups. The association between genetic alterations and patients' survival outcomes was also explored. We identified that 29.8% (48/161) and 21.4% (18/84) of patients with and without IDC-P harboured genomic alterations in DNA repair pathways, respectively (P = 0.210). Pathogenic germline DNA repair alterations were frequently detected in IDC-P carriers compared to IDC-P non-carriers (11.8% [19/161] vs 2.4% [two of 84], P = 0.024). Germline BReast CAncer type 2 susceptibility protein (BRCA2) and somatic cyclin-dependent kinase 12 (CDK12) defects were specifically identified in IDC-P carriers relative to PAC (BRCA2: 8.7% [14/161] vs 0% and CDK12: 6.8% [11/161] vs 1.2% [one of 84]). Patients with IDC-P had a distinct androgen receptor (AR) pathway alteration, characterised by an enrichment of nuclear receptor corepressor 2 (NCOR2) mutations compared with patients with pure PAC (21.1% [34/161] vs 6.0% [five of 84], P = 0.004). Increased AR alterations were detected in patients harbouring tumours with an IDC-P proportion of ≥10% vs those with an IDC-P proportion of <10% (6.4% [five of 78] vs 18.1% [15/83], P = 0.045). For IDC-P carriers, tumour protein p53 (TP53) mutation was associated with shorter castration-resistant-free survival (median 10.9 vs 28.9 months, P = 0.026), and BRCA2 alteration was related to rapid prostate-specific antigen progression for those receiving abiraterone treatment (median 9.1 vs 11.9 months, P = 0.036). Our findings provide genomic evidence explaining the aggressive phenotype of tumours with IDC-P, highlighting the potential therapeutic strategies for this patient population.

Identifiants

pubmed: 34185954
doi: 10.1111/bju.15530
doi:

Substances chimiques

Circulating Tumor DNA 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

345-355

Informations de copyright

© 2021 The Authors BJU International © 2021 BJU International Published by John Wiley & Sons Ltd.

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Auteurs

Jinge Zhao (J)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Guangxi Sun (G)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Sha Zhu (S)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Jindong Dai (J)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Junru Chen (J)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Mengni Zhang (M)

Department of Pathology, West China Hospital, Sichuan University, Chengdu, China.

Yuchao Ni (Y)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Haoran Zhang (H)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Pengfei Shen (P)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Xiaochen Zhao (X)

Departments of Biochemistry and Molecular Biology and Urology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA.

Bei Zhang (B)

Departments of Biochemistry and Molecular Biology and Urology, Mayo Clinic College of Medicine and Science, Rochester, MN, USA.

Xiuyi Pan (X)

Department of Pathology, West China Hospital, Sichuan University, Chengdu, China.

Ling Nie (L)

Department of Pathology, West China Hospital, Sichuan University, Chengdu, China.

Xiaoxue Yin (X)

Department of Pathology, West China Hospital, Sichuan University, Chengdu, China.

Jiayu Liang (J)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Xingming Zhang (X)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Zhipeng Wang (Z)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Xudong Zhu (X)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Banghua Liao (B)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Zhenhua Liu (Z)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

Cameron M Armstrong (CM)

Department of Urology, University of California Davis, Davis, CA, USA.

Allen C Gao (AC)

Department of Urology, University of California Davis, Davis, CA, USA.

Haojie Huang (H)

3DMedicines Inc., Shanghai, China.

Ni Chen (N)

Department of Pathology, West China Hospital, Sichuan University, Chengdu, China.

Hao Zeng (H)

Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, China.

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