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J. Remon



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    P1.06 - Poster Session 1 - Prognostic and Predictive Biomarkers (ID 161)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Biology
    • Presentations: 1
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      P1.06-016 - Anaplastic Lymphoma kinase (ALK) alterations by FISH in a cohort of Spanish Non-Small Cell Lung Cancer (NSCLC) patients analysed in a certified centre of reference (ID 1626)

      09:30 - 16:30  |  Author(s): J. Remon

      • Abstract

      Background
      Patients with NSCLC harbouring an ALK translocation exquisitely respond to ALK inhibitors. It is therefore important to know ALK status for newly diagnosed NSCLC patients. Our institution has become centre of reference in Spain for ALK determination by FISH for other hospitals. The aim of this work was to report the clinical and pathological characteristics of the samples with ALK results evaluated in our institution.

      Methods
      We entered clinical-pathological characteristics of external and in-house samples into a database. ALK was evaluated by FISH with the FDA approved test (Abbot Molecular Inc, Des Plaines, IL). Whole sections were analysed evaluating a minimum of 50 nuclei per case. The case was considered typically rearranged when separated green and orange/red signals (at least by three times the signal diameter) were identified and atypically rearranged when a single orange signal was observed. Gain (including both low or high genomic gain) was defined as a mean copy number of 3 to 5 fusion signals in >=10% of cells and amplification as the presence of >=6 copies of ALK per cell in >=10% of analysed cells (Salido et al, JTO 2010). To analyse correlations between ALK status and clinical-pathologic variables, we used the Chi-square test or Fisher’s exact test with a significance at p<0.05.

      Results
      A total of 471 cases were included in the database. Patients’ clinical characteristics are summarized in Table 1. ALK translocation was found in 15 of 471 patients (3.2%). Within the ALK translocated cases 8 were female, 11 were adenocarcinomas, 2 squamous cell histology, 1 large cell neuroendocrine carcinoma, and 1 not otherwise specified. There was a significant association between smoking status and ALK translocation (6.6% of translocations among non-smokers and 2% among smokers, p=0.042). Fourteen patients (3%) showed ALK amplification, 366 (77.7%) gain in ALK copy number, 50 (10.6%) were disomic and 5 (1%) monosomic for ALK and 20 cases were not evaluable (4.2%). EGFR mutation was found in 23 of 252 patients (9.1%) and non of these was observed in cases with ALK translocation. We observed an association between the type of sample and the ability to obtain an evaluable result for ALK with 97.5% assessable biopsies vs 84.4% citologies, (p<0.0001).

      N (%)
      Median age (range) 62.46 (32-91)
      Gender Male 330 (70.1)
      Female 141 (29.9)
      Smoking status Never 121 (25.7)
      Current/Former 350 (74.3)
      Sample origen Lung 425 (90.2)
      Pleura 15 (3.2)
      Lymph node 15 (3.2)
      Other 16 (3.3)
      Type of sample Citology 66 (14)
      Biopsy 405 (86)
      Stage I 104 (22)
      II 40 (8.5)
      III 87 (18.5)
      IV 240 (51)
      Histology Adenocarcinoma 363 (77.1)
      Squamous cell carcinoma 44 (9.3)
      Large cell carcinoma 11 (2.3)
      Other 43 (11.3)

      Conclusion
      ALK translocation is present in about 3% in Spanish NSCLC patients and is associated with adenocarcinoma histology and non-smoking status. The performance of ALK FISH in biopsy specimens is significantly better than in citologies.

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    P1.11 - Poster Session 1 - NSCLC Novel Therapies (ID 208)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Medical Oncology
    • Presentations: 1
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      P1.11-040 - Treatment strategies after failure to reversible Tyrosine Kinase Inhibitors (rTKI) in EGFR mutant (mut) Non-Small Cell Lung Cancer (NSCLC) patients (p). A retrospective analysis of 59 Spanish Patients (ID 2853)

      09:30 - 16:30  |  Author(s): J. Remon

      • Abstract

      Background
      Different therapeutic approaches have been used in the clinical setting in NSCLC p harbouring EGFR mutations progressing to rTKI, although the standard of care in this situation is still not well established.

      Methods
      A multinstitutional database from five different centers in Spain was review to identify EGFR mut p with acquired resistance to rTKI in order to evaluate the therapeutic strategies after rTKI failure and the effect on the post-progression survival (PPS) of these treatments.

      Results
      59 p with acquired resistance to rTKI were identified: 61% female; median (m) age 63 ±11 yrs; 96.6% Caucasian; del19 73.7%, never or light former smokers 98.3%; 93.2% adenocarcinomas; 59.4 % received TKI as first line therapy; 87% were initial stage IV. mPFS for the rTKI was 9,9 months (mo) and mOS was 32.8 mo for the entire population. P were treated with a median of 2 therapeutic strategies after the rTKI failure. 6 therapeutic strategies have been identified. As immediate approach, 31p were switched to chemotherapy (CT) with a mPPS of 5,6 mo. 10 p were switched to an irreversible TKI obtaining a mPPS of 4 mo. rTKI plus other drug was maintained in 12 p: rTKI plus CT in 9 p with a mPPS of 5,8 mo and rTKI plus other drug different to CT in 3 with a mPPS of 2 mo. Despite the progression, rTKI was maintained in 3 p, considered slow progressors obtaining a mPPS of 1,4 mo with an OS of 9mo. Furthermore, 3p with oligometastatic progressive disease local therapy was added to rTKI, obtaining mPPS of 1,4mo, but an OS of 17 mo. 4 p were treated sequentially with ≥5 strategies. These p attained a mOS of 45mo.

      Conclusion
      The combination of different strategies when treating EGFR mut p after rTKI failure may impact the survival especially when p are candidates to receive some of this treatments sequentially. These strategies may reflect different subsets of EGFR mut disease.