1288P - Efficacy of the irreversible EGFR-HER2 dual inhibitor afatinib in pretreated lung adenocarcinoma

Date 29 September 2012
Event ESMO Congress 2012
Session Poster presentation I
Topics Anti-Cancer Agents & Biologic Therapy
Non-Small-Cell Lung Cancer, Metastatic
Presenter Lorenza Landi
Authors L. Landi1, D. Galetta2, C. Bennati3, F. Currà3, R. Chiari3, G. Metro4, M. D'Arcangelo5, A. Marchetti6, F. Cappuzzo7, L. Crinò4
  • 1Oncology, Istituto Toscano Tumori, 57124 - Livorno/IT
  • 2Oncologia Medica, Istituto Tumori Giovanni Paolo II, IT-70124 - Bari/IT
  • 3Medical Oncology,, S. Maria della Misericordia Hospital,, 06132 - Perugia/IT
  • 4Oncologia Medica, S. Maria della Misericordia Hospital,, 06132 - Perugia/IT
  • 5Oncology, Istituto Toscano Tumori, Livorno/IT
  • 6Surgical Pathology, Università G.d’Annunzio, Chieti/IT
  • 7U.o. Oncologia Medica, Istituto Toscano Tumori, Livorno/IT



Although lung adenocarcinoma harboring activating Epidermal Growth Factor Receptor (EGFR) mutations respond dramatically to reversible EGFR tyrosine kinase inhibitors (TKI), all patients (pts) inevitably develop acquired resistance. Afatinib, an irreversible EGFR-HER2 dual inhibitor, demonstrated some activity in Non-Small-Cell Lung Cancer (NSCLC) pts progressing after at least 3 months of EGFR-TKI therapy.

Materials and methods

We analyzed 44 advanced lung adenocarcinoma pts resistant to EGFR-TKI according to criteria used in the LUX-Lung 1 trial (Miller VA, Lancet Oncol 2012) and treated with Afatinib at the daily dose of 40-50 mg in three Italian centers. The drug was given as compassionate use.


Pts included had a median age of 61.6 year, the majority was female (N = 23/52%), never/former smoker (N = 41/93%), with good PS (0-1; N = 37/84%) and pretreated with > 3 therapy lines (N = 36/81%). EGFR status was assessed in all cases and 35 pts (80%) harbored a mutation in exon 18 (N = 3/8.6%), in exon 19 (N = 19/54,3%), in exon 20 (T790M; N = 2/5.7%) and in exon 21 (N = 11/31.4%). Among the 42 pts evaluable for toxicity, 58% had skin rash (G3 = 4.7%) and 18% diarrhea (G3 = 2.3%). Among the 35 pts evaluable for efficacy, response rate (RR) was 11%, disease control rate (RR+ stable disease) was 65%, median progression free-survival and overall survival were 3.5 months and 4.8 months respectively. EGFR resulted mutated in 3 of 4 responders including 1 pt with T790M mutation. In 4 pts in which tumor biopsy was repeated before starting Afatinib therapy only 1 pt had T790M mutation, with no evidence of response.


In “real life” experience Afatinib showed encouraging activity in pretreated NSCLC with manageable toxicity profile.


All authors have declared no conflicts of interest.