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W. Brenner

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    P1.02 - Poster Session 1 - Novel Cancer Genes and Pathways (ID 144)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Biology
    • Presentations: 1
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      P1.02-019 - c-Met expression in unresectable or stage IV chemonaive adenocarcinoma of the lung and its co-existence with other driven mutations or genetic abnormalities. (ID 2806)

      09:30 - 16:30  |  Author(s): W. Brenner

      • Abstract

      EGFR mutation and EML4/ALK rearrangement have become standard genetic tests for patients with advanced adenocarcinoma of the lung. Other driven mutations and genetic abnormalities are still investigational including c-Met expression. c-Met overexpression has shown to confer resistance to EGFR TKI. By targeting c-Met, studies suggest that lung cancer cells may respond again to EGFR TKI therapy. The incidence of c-Met in NSCLC is not clear yet as well as how it does interact with other biomarkers.

      A retrospective study of 32 consecutive biomarker profile tests from patients with either unresectable or stage IV chemonaive adenocarcinoma of the lung were analyzed. We adopted a comprehensive biomarker panel as part of a common decision made from a lung cancer consortium. All patients’ samples were sent to Response Genetics Inc with an order to perform a panel of 9 biomarkers. We report the incidence of c-Met expression and its co-existence with other biomarkers.

      The tumor sample of 32 patients with unresectable or stage IV chemonaive adenocarcinoma of the lung were analyzed. All patients were Caucasian; gender: 18 females/14 males; median age: 76 (range, 58-89); distribution of staging was: stage I: n=3, stage II: n=1, stage III: n=7 and stage IV: n= 21 patients. c-Met was ordered in 26 patients: 9 patients had c-Met overexpressed (34%), 5 had low-expression (19%); 12 had no enough tissue for the test. None of the c-Met high expression patients had EGFR mutation; in this cohort, 4/27 patients had EML4/ALK (15%) rearrangement; 2 of them had high c-Met expression; the other 2 did not have enough tissue. The presence of K-ras (25 tumor samples tested), PI3K (25 tumor sample tested), and ROS-1 (n=26 tumor samples tested) mutations were 12/25 (48%), 1/25 (4%), and 0/26, respectively.

      Our cohort is small, and this may explain the high EML4/ALK and low EGFR incidence (sample size and patient selection). However, it is crucial to increase our knowledge on how these biomarkers interact themselves and what kind of role do they play in lung carcinogenesis. Some novel trials propose a double target approach in patients who have two pathways overexpressed. Hence, it is imperative that we develop a molecular phenotype data to understand these co-existence genetic phenomenon. Our cohort confirmed the high incidence of K-ras mutations in adenocarcinoma of the lung and also showed that c-Met high expression may be common in chemonaive patients without prior exposure to EGFR TKI. Interestingly, our 2 EML4/ALK patients also had c-Met highly expressed. PI3K and ROS-1 mutations seem to be rare genetic abnormalities.