Feasibility of targeted lymph node removal in recurrent prostate carcinoma guided by synthetic amino acid PET: Can we decrease disease burden prior to initiation of systemic therapy?

Objectives There are multiple cancers in which removal of metastatic disease including lymph nodes has proven to be of value. Yet accurately mapping prostate carcinoma nodal burden has been problematic with conventional methods. The purpose of this analysis is to determine if guided lymph node removal directed by the synthetic amino acid PET radiotracer anti-3-[18F] FACBC will affect tumor burden as reflected in lower PSA levels.

Methods Retrospective analysis of 14 patients with recurrent prostate carcinoma with nodal disease, with or without prostate bed recurrence, detected by anti-3-[18F] FACBC PET/CT who underwent either a percutaneous/incisional biopsy or surgical lymph node removal for tissue diagnosis. Pre and post-surgical PSA levels were examined.

Results 7/14 patients underwent image guided surgical lymph node removal (group 1); 7/14 had image guided percutaneous or incisional biopsy (group 2). Mean (±SD) PSA (ng/ml) at time of imaging for group 1 was 7.8(±7.9); for group 2, 7.7(± 8.0). After the procedure, mean (±SD) PSA (ng/ml) decreased in group 1 by 56% to 3.7 (±3.7); whereas PSA in group 2 increased by 73% to 11.8(±13.5), a significant difference (p<.05). Androgen deprivation therapy (ADT) was started on all patients, but at a significantly lower PSA initiation point in Group 1 than for Group 2.

Conclusions Synthetic amino acid PET/CT guided lymph node removal in recurrent prostate carcinoma is feasible and results in decreased disease burden as manifested by a statistical significant reduced PSA prior to initiation of hormonal therapy. The risk to benefit ratio of performing an additional surgical procedure versus purely non-surgical therapy is yet to be determined. A more comprehensive study is required to understand if image guided salvage dissection may be desirable in a select group of patients.

Research Support Research sponsored by the NIH (1 R01 CA 129356-01) and the Georgia Cancer Coalition