한빛사논문
- 조회348
Jeesoo Chae 1,2, Seung-Hyun Jung 3,4,5, Eun Ji Choi 6, Jae Woong Kim 5,6, Na Yung Kim 5, Sung Won Moon 5,6, Ji Youl Lee 7, Yeun-Jun Chung 1,4,5,8,* and Sug Hyung Lee 1,5,6,*
1Department of Cancer Evolution Research Center, College of Medicine, The Catholic University of Korea, 06591 Seoul, South Korea.
2Department of Biochemistry, College of Medicine, Ewha Womans University, 07804 Seoul, South Korea.
3Department of Biochemistry, College of Medicine, The Catholic University of Korea, 06591 Seoul, South Korea.
4Integrated Research Center for Genome Polymorphism, College of Medicine, The Catholic University of Korea, 06591 Seoul, South Korea.
5Department of Biomedicine & Health Sciences, College of Medicine, The Catholic University of Korea, 06591 Seoul, South Korea.
6Department of Pathology, College of Medicine, The Catholic University of Korea, 06591 Seoul, South Korea.
7Department of Urology, College of Medicine, The Catholic University of Korea, 06591 Seoul, South Korea.
8Department of Microbiology, College of Medicine, The Catholic University of Korea, 06591 Seoul, South Korea.
*Corresponding authors: correspondence to Yeun-Jun Chung or Sug Hyung Lee
Abstract
This study aimed to identify somatic mutations in nontumor cells (NSMs) in normal prostate and benign prostatic hyperplasia (BPH) and to determine their relatedness to prostate cancer (PCA). From 22 PCA patients, two prostates were sampled for 3-dimensional mapping (50 normal, 46 BPH and 1 PCA samples), and 20 prostates were trio-sampled (two normal or BPH samples and one PCA sample) and analyzed by whole-genome sequencing. Normal and BPH tissues harbored several driver NSMs and copy number alterations (CNAs), including in FOXA1, but the variations exhibited low incidence, rare recurrence, and rare overlap with PCAs. CNAs, structural variants, and mutation signatures were similar between normal and BPH samples, while BPHs harbored a higher mutation burden, shorter telomere length, larger clone size, and more private NSMs than normal prostates. We identified peripheral-zonal dominance and right-side asymmetry in NSMs, but the asymmetry was heterogeneous between samples. In one normal prostate, private oncogenic RAS-signaling NSMs were detected, suggesting convergence in clonal maintenance. Early embryonic mutations exhibited two distinct distributions, characterized as layered and mixed patterns. Our study identified that the BPH genome differed from the normal prostate genome but was still closer to the normal genome than to the PCA genome, suggesting that BPH might be more related to aging or environmental stress than to tumorigenic processes.
논문정보
- Research article
- 2024년 01월 (BRIC 등록일 2024-01-04)
- 국내 연구진
- 의약학 > 종양의학
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