PURPOSE - While the significance of circulating tumor cells (CTC) in clinically localized cancers remains controversial, it is reported that surgical tumor manipulation can increase CTC, including during open prostatectomy.
Whether this CTC "shedding" also occurs during minimally invasive prostatectomy, which minimizes tumor palpation and utilizes earlier vascular control, is unknown. Here we tested the impact of robotic-assisted laparoscopic radical prostatectomy (RALRP) on intraoperative CTC levels.
MATERIALS AND METHODS - CTC counts were compared in 8 mL peripheral blood specimens from 25 RALRP patients preoperatively versus intraoperatively after prostate excision, in addition to 11 healthy blood donors, using EpCAM immunomagnetic enrichment and multiparametric flow cytometry quantification of viable EpCAM(+)/PSMA(+)/CD45(-) cells. Intraoperative CTC counts and increases were tested in univariable analyses for association with perioperative variables, histopathology and postoperative progression.
RESULTS - CTC were detected in 0% of healthy controls compared to 48% and 52% of RALRP patients preoperatively and intraoperatively, respectively (range 1-8 cells). There was no difference in incidence or mean number of CTC preoperatively versus intraoperatively. Intraoperative CTC increases versus decreases were equally infrequent (20% each), with no intraoperative increases of >1 CTC, and 60% of patients had no intraoperative change from preoperative levels. Intraoperative CTC detection was not significantly associated with RALRP operative characteristics, histopathology or early postoperative progression with a median 21 month follow-up.
CONCLUSIONS - RALRP does not cause significant intraoperative increases in CTC, in contrast to historical reports on open prostatectomy. These findings may aid urologists in counseling RALRP candidates regarding the possibility of intraoperative tumor cell shedding.
The Journal of urology. 2015 Nov 12 [Epub ahead of print]
Eric C Kauffman, Min-Jung Lee, Sylvia V Alarcon, Sunmin Lee, Anthony N Hoang, Annerleim Walton Diaz, Raju Chelluri, Srinivas Vourganti, Jane B Trepel, Peter A Pinto
Urologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD; Departments of Urology and Cancer Genetics, Roswell Park Cancer Institute, Buffalo, NY. Developmental Therapeutics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. , Developmental Therapeutics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. , Developmental Therapeutics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. , Urologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. , Urologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. , Urologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. , Urologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD; Department of Urology, State University of New York, Upstate Medical University, Syracuse, NY. , Developmental Therapeutics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. , Urologic Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD.