CTC Number May Be Marker of Improved Survival in Metastatic Castration-Resistant Prostate Cancer


Key Points

  • CTC nonzero at baseline and 0 at 13 weeks (CTC0) and CTC conversion (≥ 5 CTCs at baseline, ≤ 4 at 13 weeks) were the best discriminators of longer overall survival.
  • The CTC0 measure was applicable to more patients.

In a study reported in the Journal of Clinical Oncology, Heller et al identified two circulating tumor cell (CTC) markers that had high discriminatory ability for improved survival in metastatic castration-resistant prostate cancer.

Study Details

The study used individual patient data from 5 randomized trials involving 6,081 patients with metastatic castration-resistant prostate cancer to analyze the association of 8 week-13 CTC and prostate-specific antigen (PSA) markers with survival: CTC nonzero at baseline and 0 at 13 weeks (CTC0), CTC conversion (≥ 5 CTCs at baseline, ≤ 4 at 13 weeks; U.S. Food and Drug Administration–cleared response measure), 30%, 50%, and 70% decreases in CTC count, and 30%, 50%, and 70% decrease in PSA level. Patients with missing week-13 data were considered nonresponders.

Best Markers

CTC0 and CTC conversion had the highest-weighted C indices and smaller standard deviations (SDs) for association with prolonged overall survival among the markers analyzed. Mean C indices (SD) were 0.81 (0.04) for CTC0; 0.79 (0.03) for CTC conversion; 0.72 (0.06), 0.72 (0.06), and 0.73 (0.05) for 30%, 50%, and 70% decrease in CTC count; and 0.71 (0.03), 0.72 (0.06), and 0.74 (0.05) for 30%, 50%, and 70% decrease in PSA level.

Overall, 75% of eligible patients could be evaluated with the CTC0 endpoint vs 51% with the CTC conversion endpoint.

The investigators concluded, “The CTC0 and CTC conversion endpoints had the highest discriminatory power for overall survival. Both are robust and meaningful response endpoints for early-phase metastatic castration-resistant prostate cancer clinical trials. CTC0 is applicable to a significantly higher percentage of patients than CTC conversion.”

The study was supported by grants from the National Institutes of Health, Sidney Kimmel Center for Prostate and Urologic Cancers, Prostate Cancer Foundation, Department of Defense Prostate Cancer Research Program, and Janssen Diagnostics, a division of Janssen Pharmaceutica NV.

Howard I. Scher, MD, of Sidney Kimmel Center for Prostate and Urologic Cancers at Memorial Sloan Kettering Cancer Center, is the corresponding author for the Journal of Clinical Oncology article. 

The content in this post has not been reviewed by the American Society of Clinical Oncology, Inc. (ASCO®) and does not necessarily reflect the ideas and opinions of ASCO®.




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