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C. Choi



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    P3.10 - Poster Session 3 - Chemotherapy (ID 210)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Medical Oncology
    • Presentations: 1
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      P3.10-027 - Selection of patients with adenocarcinoma of the lung for Gefinitib by FDG PET metabolic response (ID 1628)

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

      • Abstract

      Background
      Gefitinib is the standard therapy for non-small cell lung cancer patients harboring activating EGFR mutation. However, there are some limitations; 1) we need sufficient tumor tissue to analyze EGFR mutation test; 2) we have to wait result of the test, causing delay of treatment; and 3) we can evaluate the response 4 weeks later but some of the patients do not respond to EGFR TKIs even though they have an activating EGFR mutation. Therefore, we investigated the role of FDG PET as a method overcoming the limitations to evaluate the response to EGFR TKIs.

      Methods
      Key eligibility is as follows; advanced/metastatic adenocarcinoma of the lung; never smoker; no prior chemotherapy; ECOG PS of 0-1; and main lesion > 2cm. The patients performed two times of FDG PET; before starting gefitinib and after 7 days of gefitinib 250mg/d therapy. If % decrease of peak standardized uptake value (pSUV) of main lesion was 20% or more, gefitinib was continued till progression (Group A). After 6 weeks of the treatment, conventional response evaluation using chest CT was done. But, if % decrease of pSUV less than 20% or increase, treatment changed from gefitinib to pemetrexed/cisplatin (Group B). Primary endpoint was to see the response rate of gefitinib in the patients of Group A. EGFR mutation test using direct sequencing method was also performed but the result was not available or unknown to investigators before the report of second PET result.

      Results
      Between Apr 2012 and Apr 2013, 50 patients participated. After 7 day-treatment of gefitinib, 28 out of 50 patients showed decrease of pSUV of main lesion ≥ 20 % (47.4±15.8%) (Group A). Out of the 28 patients in Group A, 27 patients were evaluable; PR in 24 (85.7%), SD in 2 and PD in 1 (Table). EGFR mutation was identified later in 24 patients (85.7%) and 4 patients showed wild type EGFR with 2 PRs, 1 PD and 1 NE. Twenty-two patients showed decrease of pSUV < 20 % or increase (-0.3±15.3%). Interestingly, 19 patients (86.4%) had wild type EGRF while two had an activating EGFR mutation. One patient who showed mutated EGFR in Group B was given gefitinib continuously as physician’s decision. But the patient did progressed after all.

      Group A (gefitinib, n=28) Group B (pem/cis, n=22)
      Response EGFR mutation EGFR mutation
      Postive (n=24) Negative (n=4) Total (n=28) Postive (n=2) Negative (n=19) NE (n=1) Total (n=22)
      CR - - 0 - - - 0
      PR 22 2 24 (85.7%) 1 13 - 14 (63.6%)
      SD 2 - 2 (7.1%) - 4 - 4 (18.2%)
      PD - 1 1 (3.6%) - 1 - 1 (4.5%)
      NE - 1 1 (3.6%) 1 1 1 3 (13.6%)

      Conclusion
      The % decrease of pSUV of ≥ 20 % after 7 days of gefitinib treatment would be a good indicator to predict tumor response to EGFR TKI therapy in this clinical setting.

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    P3.19 - Poster Session 3 - Imaging (ID 181)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Imaging, Staging & Screening
    • Presentations: 1
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      P3.19-009 - Newly developed early lung cancer during follow-up of idiopathic interstitial pneumonia: serial HRCT observations (ID 1719)

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

      • Abstract

      Background
      To describe HRCT findings of newly developed peripheral T1 lung cancer in idiopathic interstitial pneumonia (IIP) during IIP follow-up

      Methods
      Between November 2001 and October 2012, 66 consecutive patients (62men, 4 women; median age 64, range 40~85 years) who were diagnosed as IIP, fulfilled the American Thoracic Society diagnostic criteria and new cancer (including fourteen small cell) simultaneously, were included. Two radiologists independently reviewed 132 serial CT scans of 66 patients, determined the earliest scan showing lung cancer, and evaluated tumor size (mm), lobar location, axial location on transverse image, shape, and density of tumor. The median interval between null-IIP to new cancer-IIP was measured. Delay in diagnosis was measured from the time of the earliest scan showing lung cancer and the subsequent clinical diagnosis. Formal radiologic reports as ‘first choice’ before diagnosis of cancer were reviewed.

      Results
      The inter-observer agreement was good (Kappa value > 0.77). The median smallest tumor size on axial scan at presentation was 17mm (± 6.57, range, 5-30mm) with T1a/T1b (48/18). Tumor was most commonly located in right lower lobe (29/66, 43.9%), followed by left lower lobe (13, 19.7%). Thirty five tumors (53.0%) were in the interface between normal and fibrotic lung cysts such as honeycomb cysts, twenty two (33.3%) were in the midst of fibrotic lung cysts, and nine (13.6%) were in the normal lung. Fifty nine (83.3%) tumors had round or oval shape, seven (10.6%) tumors had a stellate shape, and two had a band-like shape. Most of the tumors (90.3%) presented as solid density rather than part solid, ground-glass opacity or consolidation. Lung cancers were found during the mean follow-up CT period of 513 days. The median delay in diagnosis was 440 days. Most of the lesions (70%) were interpreted as lung cancer, but nine were interpreted as pneumonia or fungal infection and seven were missed (10.6%) on HRCT.

      Conclusion
      About one third of the tumors were misdiagnosed including missed in ten percents. Over fifty percent of the cancers are located at the interface between normal lung and fibrotic cysts. New lung cancers usually show as tumor with a round or oval shape and solid density.