Author of

• 10801

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  P1.11 - Poster Session 1 - NSCLC Novel Therapies (ID 208)

  • Event: WCLC 2013
  • Type: Poster Session
  • Track: Medical Oncology
  • Presentations: 1
  • Moderators:
  • Coordinates: 10/28/2013, 09:30 - 16:30, Exhibit Hall, Ground Level

  • 10840

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    P1.11-040 - Treatment strategies after failure to reversible Tyrosine Kinase Inhibitors (rTKI) in EGFR mutant (mut) Non-Small Cell Lung Cancer (NSCLC) patients (p). A retrospective analysis of 59 Spanish Patients (ID 2853)

    09:30 - 09:30  |  Author(s): D. Alcaraz
    • Abstract

    Background
    Different therapeutic approaches have been used in the clinical setting in NSCLC p harbouring EGFR mutations progressing to rTKI, although the standard of care in this situation is still not well established.

    Methods
    A multinstitutional database from five different centers in Spain was review to identify EGFR mut p with acquired resistance to rTKI in order to evaluate the therapeutic strategies after rTKI failure and the effect on the post-progression survival (PPS) of these treatments.

    Results
    59 p with acquired resistance to rTKI were identified: 61% female; median (m) age 63 ±11 yrs; 96.6% Caucasian; del19 73.7%, never or light former smokers 98.3%; 93.2% adenocarcinomas; 59.4 % received TKI as first line therapy; 87% were initial stage IV. mPFS for the rTKI was 9,9 months (mo) and mOS was 32.8 mo for the entire population. P were treated with a median of 2 therapeutic strategies after the rTKI failure. 6 therapeutic strategies have been identified. As immediate approach, 31p were switched to chemotherapy (CT) with a mPPS of 5,6 mo. 10 p were switched to an irreversible TKI obtaining a mPPS of 4 mo. rTKI plus other drug was maintained in 12 p: rTKI plus CT in 9 p with a mPPS of 5,8 mo and rTKI plus other drug different to CT in 3 with a mPPS of 2 mo. Despite the progression, rTKI was maintained in 3 p, considered slow progressors obtaining a mPPS of 1,4 mo with an OS of 9mo. Furthermore, 3p with oligometastatic progressive disease local therapy was added to rTKI, obtaining mPPS of 1,4mo, but an OS of 17 mo. 4 p were treated sequentially with ≥5 strategies. These p attained a mOS of 45mo.

    Conclusion
    The combination of different strategies when treating EGFR mut p after rTKI failure may impact the survival especially when p are candidates to receive some of this treatments sequentially. These strategies may reflect different subsets of EGFR mut disease.