Author of

• 12648

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  P3.11 - Poster Session 3 - NSCLC Novel Therapies (ID 211)

  • Event: WCLC 2013
  • Type: Poster Session
  • Track: Medical Oncology
  • Presentations: 1
  • Moderators:
  • Coordinates: 10/30/2013, 09:30 - 16:30, Exhibit Hall, Ground Level

  • 12652

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    P3.11-004 - A Prospective Study of the Use of Circulating Markers as Predictors for Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor Treatment in Pulmonary Adenocarcinoma (ID 726)

    09:30 - 09:30  |  Author(s): P. Tseng
    • Abstract

    Background
    The use of liquid tissue, such as circulating cells or free DNA, to predict treatment response is attracting more attention.

    Methods
    Patients with stage IV adenocarcinoma of the lungs who were going to receive gefitinib or erlotinib treatment were included. Both tumor tissue and plasma specimens were prospectively collected before treatment and analyzed using the ARMS-Scorpions method for EGFR mutation status analysis. The numbers of circulating CD146+/CD3- cells (as circulating endothelial cells, CECs), CD34+/CD45- cells (as endothelial progenitor cells, EPCs), and CD133+ cells (as circulating cancer stem cells, CSCs) were measured with flow cytometry. From June 2010 to July 2012, 112 consecutive patients were enrolled.

    Results
    Eighty of the 112 patients had tissue EGFR (tEGFR) activating mutations. Plasma EGFR (pEGFR) activating mutations were detected in 24 of 80 patients with tEGFR activating mutations. There were lower CEC, EPC, and CSC counts in tEGFR mutated patients than in wild-type patients (p=0.001, 0.012, and 0.001, respectively). Progression-free survival (PFS) was best in those with only tEGFR mutations (n=56, median 16.8 months), followed by those with both tEGFR and pEGFR mutations (n=24, median 7.9 months), and worst in EGFR wild-type patients (n=32, median 2.1 months) (p<0.0001). PFS was significantly longer in patients with low CEC and low CSC counts than in those with high cell counts (p=0.0023 and 0.0053, respectively). Multivariate analysis showed that the presence of pEGFR was a poor prognostic factor, but not the presence of other markers.

    Conclusion
    The presence of pEGFR mutation is a poor prognostic factor for patients with tEGFR mutations when they receive EGFR-TKI treatment. EGFR wild-type patients had higher counts of CECs, EPCs, and CSCs. These circulating markers are useful in predicting EGFR-TKI treatment efficacy, but less useful than pEGFR detection.