Is lymphovascular invasion a powerful predictor for biochemical recurrence in pT3 N0 prostate cancer? Results from the K-CaP database

Yong Hyun Park, Yejin Kim, Hwanjo Yu, In Young Choi, Seok Soo Byun, Cheol Kwak, Byung Ha Chung, Hyun Moo Lee, Choung Soo Kim, Ji Youl Lee

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14 Citations (Scopus)

Abstract

To assess the impact of lymphovascular invasion (LVI) on the risk of biochemical recurrence (BCR) in pT3 N0 prostate cancer, clinical data were extracted from 1,622 patients with pT3 N0 prostate cancer from the K-CaP database. Patients with neoadjuvant androgen deprivation therapy (n = 325) or insufficient pathologic or follow-up data (n = 87) were excluded. The primary endpoint was the oncologic importance of LVI, and the secondary endpoint was the hierarchical relationships for estimating BCR between the evaluated variables. LVI was noted in 260 patients (21.5%) and was significantly associated with other adverse clinicopathologic features. In the multivariate Cox regression analysis, LVI was significantly associated with an increased risk of BCR after adjusting for known prognostic factors. In the Bayesian belief network analysis, LVI and pathologic Gleason score were found to be first-degree associates of BCR, whereas prostate-specific antigen (PSA) level, seminal vesicle invasion, perineural invasion, and high-grade prostatic intraepithelial neoplasia were considered second-degree associates. In the random survival forest, pathologic Gleason score, LVI, and PSA level were three most important variables in determining BCR of patients with pT3 N0 prostate cancer. In conclusion, LVI is one of the most powerful adverse prognostic factors for BCR in patients with pT3 N0 prostate cancer.

Original languageEnglish
Article number25419
JournalScientific reports
Volume6
DOIs
Publication statusPublished - 2016 May 5

Bibliographical note

Funding Information:
This work was supported by the Korean Prostate Bank supported by the National Research Foundation funded by the Ministry of Science, ICT and Future Planning, Korea (NRF-2012M3A9B8021691).

Publisher Copyright:
© 2016, Nature Publishing Group. All rights reserved.

All Science Journal Classification (ASJC) codes

  • General

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