Abstract 2240: Clinical significance of CEA, PRL3 and EZH2 transcripts expressed in lymph nodes of colorectal cancer patients

Objective: The role of micrometastases detected immunologically and molecularly in lymph nodes of colorectal cancer patients remains elusive. We investigated the prognostic significance of CEA, PRL3 and EZH2 expressed in lymph nodes of 42 pathologically node-negative (pN0) colorectal patients and 13 stage III/IV patients as controls. Seventeen pN0 patients (40%) received adjuvant therapy after curative surgery. Experimental design: CEA, PRL3 and EZH2 transcripts were amplified by reverse transcription PCR in nearly 600 paraffin embedded lymph nodes. On average 9.7 ± 5.7 nodes were harvested per case. After 55 months median follow-up, gene expression was correlated with recurrence-free (RFS), overall (OS) and disease-free survival (DFS), using Kaplan-Meier analysis and log-rank test for comparison. Results: The proportion of cases demonstrating CEA+, PRL3+ and EZH2+lymph node expression increased from stage I to III/IV and reached 71%, 76% and 26% respectively in the pN0 group. EZH2 had no significant prognostic value among pN0 patients. Disease progressed more rapidly (50% DFS at 30 versus 53 months) in EZH2+ than EZH2- node-positive patients. CEA+ was associated with ∼18% lower RFS/OS, and 8% lower DFS than CEA- among therapeutically-untreated patients, those with colon and with stage II tumors. pN0 patients with PRL3+ nodes had better outcomes than PRL3- cases (DFS, P= 0.059), namely in the colorectal (OS, P= 0.056; DFS, P= 0.12), colon (DFS, P= 0.056) and stage II tumor in the non-adjuvant settings (DFS, P= 0.0047). Conclusions: Lymph node expression of the PRL3 phosphatase gene predicted more favorable outcomes for pN0 colorectal cancer patients. The role of CEA as an adverse predictor of survival was confirmed albeit less significant than previously reported. Neither CEA nor PRL3 nodal expression was predictive of rectal cancer recurrence. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2240.