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M. Sawicki
Author of
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P2.03b - Poster Session with Presenters Present (ID 465)
- Event: WCLC 2016
- Type: Poster Presenters Present
- Track: Advanced NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 12/06/2016, 14:30 - 15:45, Hall B (Poster Area)
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P2.03b-011 - Screening for ALK Abnormalities in Central Nervous System Metastases of Non-Small-Cell Lung Cancer (ID 5146)
14:30 - 14:30 | Author(s): M. Sawicki
- Abstract
Background:
Anaplastic lymphoma kinase (ALK) gene rearrangement was reported in 3-7% of primary non-small-cell lung cancer (NSCLC) and its presence is commonly associated with adenocarcinoma (AD) type and non-smoking history. ALK tyrosine kinase inhibitors (TKIs) such as crizotinib, alectinib and ceritinib showed efficiency in patients with primary NSCLC harboring ALK gene rearrangement. Moreover, response to ALK TKIs was observed in central nervous system (CNS) metastatic lesions of NSCLC. Till date there is limited data ALK rearrangement incidence in CNS metastases of NSCLC, which could be considered as a regiment for targeted treatment. For this reason we undertook the present retrospective study to determine the frequency of ALK abnormalities in CNS metastases of NSCLC.
Methods:
The studied group included 145 patients (45 females, 100 males, median age 60 years ±8) with CNS metastases of NSCLC. The studied group was heterogeneous in terms of histology (80 adenocarcinoma, 29 squamous-cell carcinoma, 22 large-cell carcinoma, 14 not otherwise specific) and smoking status. ALK abnormalities were screened in sections obtained from formalin fixed paraffin embedded (FFPE) tissue samples. NSCLC using immunohistochemical (IHC) automated staining (BenchMark GX, Ventana, USA) and fluorescence in situ hybridization (FISH) technique (Abbot Molecular, USA).
Results:
ALK abnormalities were detected in 4.8% (7/145) of CNS metastases of NSCLC. ALK abnormalities were observed in AD and squamous-cell carcinoma (SqCC) patients (7.5%; 6/80 vs. 3.4%; 1/29, respectively). Analysis of clinical and demographic factors indicated that expression of abnormal ALK was significantly more frequently observed (p=0.0002; χ[2]=16.783) in former-smokers. Comparison of IHC and FISH results showed some discrepancies, which were caused by unspecific staining of macrophages and glial/nerve cells, which constitute the background of CNS tissues.
Conclusion:
In this retrospective study we evaluated the expression of ALK abnormal protein and ALK gene rearrangement in extremely unique material which are CNS metastatic lesions of NSCLC. The frequency of ALK abnormalities in this material could be higher or comparable to frequency of ALK gene rearrangement in primary NSCLC tumors. However, the comparison of IHC and FISH results showed discrepancies that arose from unspecific background, which was made by cells with nonmalignant origin. For this reason assessment of ALK gene rearrangement in CNS tissues require additional standardizations.
