Author of

• 16549

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  P1.02 - Poster Session with Presenters Present (ID 454)

  • Event: WCLC 2016
  • Type: Poster Presenters Present
  • Track: Biology/Pathology
  • Presentations: 1
  • Moderators:
  • Coordinates: 12/05/2016, 14:30 - 15:45, Hall B (Poster Area)

  • 16584

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    P1.02-035 - Concomitant Driver Mutation Determines Tumor Growth in EGFR Mutation-Positive Lung Adenocarcinoma (ID 5397)

    14:30 - 14:30  |  Author(s): H. Kuwano
    • Abstract

    Background:
    In the practice of precision medicine, understanding tumor characteristics in the individual patient is crucial. The aim of this study was to analyze tumor aggressiveness from two perspectives: actual growth rate calculated from the tumor; and molecular profiles obtained by next-generation sequencing.
    
    Methods:
    Participants comprised patients who underwent preoperative CT two or more times. DNA and RNA of 10 lung adenocarcinoma tumor samples were extracted. Whole-exome and -transcriptome data were obtained, and somatic mutations were detected. Preoperative CT scans were retrospectively reviewed and volume doubling time (VDT) of each tumor was calculated using a modified Schwarz equation.
    
    Results:
    Median VDT was 104 days (range, 42-653 days). Median number of somatic missense mutations was 20 (range, 7-306). EGFR mutations were present in 6 patients. Patients were divided into two groups by VDT for further analyses: Slow group with VDT ≥104 days (n=5); and Rapid Group with VDT <104 days (n=5). All patients with EGFR mutation without concomitant KRAS mutation were in the Slow Group. In contrast, a patient with concomitant mutations of EGFR and KRAS showed a considerably rapid growing tumor with a VDT of 45 days. A patient with concomitant mutations in EGFR and PIK3CA had a relatively slow-growing tumor, although VDT was the shortest in the Slow Group (120 days). Figure 1
    
    
    
    Conclusion:
    EGFR mutation was associated with slow growth of the tumor, although the growth rate may be influenced by concomitant mutation of other driver genes. This may be one of the reasons that the clinical response of tyrosine kinase inhibitors are poor in some patients with EGFR mutation. Assessment of tumor aggressiveness by molecular profiling and by sequential CT are both important for the practice of precision medicine.