Harun Fajkovic1, Romain Mathieu2, Ilaria Lucca3, Manuela Hiess4, Nicolai Hübner4, Bashir Al Hussein Al Awamlh5, Richard Lee5, Alberto Briganti6, Pierre Karakiewicz7, Yair Lotan8, Morgan Roupret9, Michael Rink10, Luis Kluth10, Wolfgang Loidl11, Christian Seitz4, Tobias Klatte4, Gero Kramer4, Martin Susani12, Shahrokh F Shariat13. 1. Department of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna General Hospital, Vienna, Austria. Electronic address: harun.fajkovic@gmail.com. 2. Department of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna General Hospital, Vienna, Austria; Department of Urology, Rennes University Hospital, Rennes, France. 3. Department of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna General Hospital, Vienna, Austria; Department of Urology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. 4. Department of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna General Hospital, Vienna, Austria. 5. Department of Urology, Weill Medical College of Cornell University, New York-Presbyterian Hospital, New York, NY. 6. Department of Urology, Urological Research Institute, San Raffaele Scientific Institute, Milan, Italy. 7. Cancer Prognostics and Health Outcomes Unit, University of Montreal Health Centre, Montreal, Quebec, Canada. 8. Department of Urology, University of Texas Southwestern Medical Center, Dallas, TX. 9. Department of Urology, Pitié-Salpétrière Hospital, Paris, France. 10. Department of Urology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. 11. Department of Urology, St. Vincent´s Hospital, Linz, Austria. 12. Department of Pathology, Medical University of Vienna, Vienna, Austria. 13. Department of Urology, Comprehensive Cancer Center, Medical University of Vienna, Vienna General Hospital, Vienna, Austria; Department of Urology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland; Department of Urology, University of Texas Southwestern Medical Center, Dallas, TX.
Abstract
OBJECTIVE: To validate the impact of lymphovascular invasion (LVI) on biochemical recurrence (BCR) in patients treated with radical prostatectomy (RP) in a large multiinstitutional cohort. MATERIAL AND METHODS: Retrospective data from 6,678 patients treated with a RP and bilateral lymphadenectomy for prostate cancer (PC) from 8 centers were collected. The primary endpoint was BCR. RESULTS: Overall, 767 patients (11.5%) had LVI. Patients with LVI had significantly higher Gleason scores (P = 0.01). After a median follow-up of 28 months (interquartile range: 21-44), patients with LVI had a 1.66 fold increased risk of BCR (P<0.001). The 1-, 2- and 5-year biochemical recurrence-free survival probabilities for LVI vs. no LVI were 94% vs. 97%, 91% vs. 94%, and 76% vs. 84%, respectively. On multivariable analysis that adjusted for the effects of established prognostic factors, LVI was an independent predictor of BCR (hazard ratio = 1.42, P<0.001). Adding LVI to a multivariable base model increased the discrimination by a small but significant margin (+0.2%, P = 0.0005). In subgroup analyses, LVI remained an independent predictor for BCR in patients with worse pathological features. CONCLUSIONS: About 10% of patients with localized PC have LVI on their RP specimen. We confirm that LVI is associated with features of biologic aggressive PC such as high Gleason grade and BCR after RP. Adverse further studies with strict definitions of LVI and longer follow-up periods are needed to determine the prognostic and predictive utility of LVI in the management of PC.
OBJECTIVE: To validate the impact of lymphovascular invasion (LVI) on biochemical recurrence (BCR) in patients treated with radical prostatectomy (RP) in a large multiinstitutional cohort. MATERIAL AND METHODS: Retrospective data from 6,678 patients treated with a RP and bilateral lymphadenectomy for prostate cancer (PC) from 8 centers were collected. The primary endpoint was BCR. RESULTS: Overall, 767 patients (11.5%) had LVI. Patients with LVI had significantly higher Gleason scores (P = 0.01). After a median follow-up of 28 months (interquartile range: 21-44), patients with LVI had a 1.66 fold increased risk of BCR (P<0.001). The 1-, 2- and 5-year biochemical recurrence-free survival probabilities for LVI vs. no LVI were 94% vs. 97%, 91% vs. 94%, and 76% vs. 84%, respectively. On multivariable analysis that adjusted for the effects of established prognostic factors, LVI was an independent predictor of BCR (hazard ratio = 1.42, P<0.001). Adding LVI to a multivariable base model increased the discrimination by a small but significant margin (+0.2%, P = 0.0005). In subgroup analyses, LVI remained an independent predictor for BCR in patients with worse pathological features. CONCLUSIONS: About 10% of patients with localized PC have LVI on their RP specimen. We confirm that LVI is associated with features of biologic aggressive PC such as high Gleason grade and BCR after RP. Adverse further studies with strict definitions of LVI and longer follow-up periods are needed to determine the prognostic and predictive utility of LVI in the management of PC.
Authors: Trevor A Flood; Nicola Schieda; Jordan Sim; Rodney H Breau; Chris Morash; Eric C Belanger; Susan J Robertson Journal: Virchows Arch Date: 2017-10-03 Impact factor: 4.064
Authors: William Gesztes; Cara Schafer; Denise Young; Jesse Fox; Jiji Jiang; Yongmei Chen; Huai-Ching Kuo; Kuwong B Mwamukonda; Albert Dobi; Allen P Burke; Judd W Moul; David G McLeod; Inger L Rosner; Gyorgy Petrovics; Shyh-Han Tan; Jennifer Cullen; Shiv Srivastava; Isabell A Sesterhenn Journal: Sci Rep Date: 2022-03-30 Impact factor: 4.996