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C. Roe



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    P2.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 234)

    • Event: WCLC 2015
    • Type: Poster
    • Track: Biology, Pathology, and Molecular Testing
    • Presentations: 1
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      P2.04-030 - Activating and Resistance Mutations of EGFR in Peruvian Patients with Metastatic NSCLC (ID 380)

      09:30 - 09:30  |  Author(s): C. Roe

      • Abstract
      • Slides

      Background:
      The evaluation of EGFR mutational status of the EGFR in non-small cell lung cancer (NSCLC) is crucial to select the adequate targeted therapy and to know the prognostic of patients. Our aim was describe to determine the frequency of activating and resistance mutations of EGFR in a large cohort of Peruvian patients.

      Methods:
      We tested metastatic tumor samples from 436 NSCLC patients for known EGFR mutations involving exon 18 (G719X), exon 19 (deletions), exon 20 (T790M, S768I and insertions) and exon 21 (L858R). Samples were from a mutational testing program sponsored by a pharmaceutical company. All samples were processed at a central reference laboratory (Roe laboratory, Lima-Peru) under protocolized laboratory procedures.

      Results:
      A total of 398 out of 436 samples were evaluable for determination of EGFR mutational status. Fifty five percent of patients were male. EGFR mutations was present in 36.7% of cases (n = 146). In regard to specific mutations, G719X (in exon 18) was present in 1% (n = 4); deletions in exon 19 had a frequency of 19.6% (n = 78). Mutations in exon 20 were present in 3.5% (n = 14). In patients with exon 20 mutated, 8 cases had insertions, 5 cases had the mutation T790M and 1 case had the mutation S768I. Mutation L858R (exon 21) in 14.1% (n = 56) of cases. Coexistence of two mutations were present in exon 19/exon 20 (n = 3) and exon 20/ exon 21 (n = 3). Female patients were more likely to have any EGFR mutation with a Relative Risk = 1.92 and a P < 0.001, in the Chi-square test. In tumors with EGFR mutated. The sensible profile for EGFR tyrosine kinase inhibitors (TKI´s) was present in 94.5% of cases (n=138) while 8 cases (5.5%) had mutations associated with resistance to TKI´s.

      Conclusion:
      Most patients with metastatic NSCLC and EGFR mutations will benefit from anti-EGFR targeted therapy. Our frequency of EGFR activating or resistance mutation was similar to other Latin American countries where mutations in exon 19 are the most frequent.

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