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Transl Oncol. 2019 Jan;12(1):43-48. doi: 10.1016/j.tranon.2018.09.003. Epub 2018 Sep 25.

Biomarkers Associated with Tumor Heterogeneity in Prostate Cancer.

Author information

1
Samsung Genome Institute, Samsung Medical Center, Seoul 06351, Republic of Korea; Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences & Technology, Sungkyunkwan University, Seoul 06351, Republic of Korea.
2
Center for Health Promotion, Samsung Medical Center, Seoul, Republic of Korea.
3
Samsung Genome Institute, Samsung Medical Center, Seoul 06351, Republic of Korea.
4
Samsung Genome Institute, Samsung Medical Center, Seoul 06351, Republic of Korea; Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences & Technology, Sungkyunkwan University, Seoul 06351, Republic of Korea; Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon 16419, Republic of Korea.
5
Samsung Genome Institute, Samsung Medical Center, Seoul 06351, Republic of Korea. Electronic address: jegun.joung@samsung.com.
6
Center for Health Promotion, Samsung Medical Center, Seoul, Republic of Korea. Electronic address: jyuro.jeong@samsung.com.

Abstract

BACKGROUND:

Prostate cancers exhibit intratumor heterogeneity (ITH), like other cancer types. The ITH may affect diverse phenotypes such as treatment response, drug resistance, and clinical outcomes. It is crucial to consider ITH to understand tumorigenesis.

METHODS:

Genomic and transcriptomic profiles of prostate cancer patients were investigated to determine which markers are correlated with the degree of tumor heterogeneity. In addition, the correlation between the immune activity and clonality of tumors was examined.

RESULTS:

Tumor heterogeneity across all prostate cancer samples was variable. However, ITH events were dependent on genomic and clinical features. Interestingly, prostate-specific antigen score increased in tumors with multiple subclones, indicating high-grade tumor heterogeneity. On the other hand, CD8-positive T-cell activation decreased in highly heterogeneous tumors. Intriguingly, PTEN deletion was prominently enriched in high heterogeneity groups, with a strong association with heterozygous loss. Expression of major genes including PTEN, CDC42EP5, RNLS, GP2, NETO2, and AMPD3 was closely related to tumor heterogeneity in association with PTEN deletion.

CONCLUSIONS:

In prostate cancer, ITH, a potential factor affecting tumor progression, is associated with PTEN deletion and cytotoxic T cell inactivation.

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