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High serum level of C-reactive protein is associated with worse outcome of patients with advanced-stage NSCLC treated with erlotinib

O. Fiala, M. Pesek, J. Finek, O. Topolcan, J. Racek, M. Minarik, L. Benesova, Z. Bortlicek, A. Poprach, T. Buchler,

. 2015 ; 36 (12) : 9215-22. [pub] 20150619

Language English Country Netherlands

Document type Journal Article, Research Support, Non-U.S. Gov't

Persistent link   https://www.medvik.cz/link/bmc16020658

Erlotinib is a low molecular weight tyrosine kinase inhibitor (TKI) directed at epidermal growth factor receptor (EGFR), widely used in the treatment of locally advanced or metastatic-stage non-small cell lung cancer (NSCLC). Although introduction of EGFR-TKIs have significantly extended survival of advanced-stage NSCLC patients, their efficacy in the entire patient population is relatively low. Aside from activating EGFR mutations, no reliable biochemical or molecular predictors of response to erlotinib have been established. The aim of our retrospective study was to evaluate the association of baseline serum levels of C-reactive protein (CRP) with outcomes in patients with advanced-stage NSCLC treated with erlotinib. We retrospectively analyzed clinical data of 595 patients with advanced-stage NSCLC (IIIB or IV) treated with erlotinib. Serum CRP was measured using an immunoturbidimetric method. High baseline levels of CRP (≥10 mg/l) were measured in 387 (65 %) patients, and normal levels (<10 mg/l) were measured in 208 (35 %) patients. The median progression-free survival (PFS) and overall survival (OS) for patients with high CRP was 1.8 and 7.7 compared to 2.8 and 14.4 months for patients with low CRP (p < 0.001 and p < 0.001). The multivariable Cox proportional hazards model revealed that CRP was significantly associated with PFS and also with OS (hazard ratio (HR) = 1.57, p < 0.001, and HR = 1.63, p < 0.001, respectively). In conclusion, the results of the conducted retrospective study suggest that high baseline level of CRP was independently associated with worse outcome of patients with advanced-stage NSCLC treated with erlotinib. CRP is a commonly used biomarker which is simple and easy to detect, and thus, it is feasible for the use in the routine clinical practice.

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$a Erlotinib is a low molecular weight tyrosine kinase inhibitor (TKI) directed at epidermal growth factor receptor (EGFR), widely used in the treatment of locally advanced or metastatic-stage non-small cell lung cancer (NSCLC). Although introduction of EGFR-TKIs have significantly extended survival of advanced-stage NSCLC patients, their efficacy in the entire patient population is relatively low. Aside from activating EGFR mutations, no reliable biochemical or molecular predictors of response to erlotinib have been established. The aim of our retrospective study was to evaluate the association of baseline serum levels of C-reactive protein (CRP) with outcomes in patients with advanced-stage NSCLC treated with erlotinib. We retrospectively analyzed clinical data of 595 patients with advanced-stage NSCLC (IIIB or IV) treated with erlotinib. Serum CRP was measured using an immunoturbidimetric method. High baseline levels of CRP (≥10 mg/l) were measured in 387 (65 %) patients, and normal levels (<10 mg/l) were measured in 208 (35 %) patients. The median progression-free survival (PFS) and overall survival (OS) for patients with high CRP was 1.8 and 7.7 compared to 2.8 and 14.4 months for patients with low CRP (p < 0.001 and p < 0.001). The multivariable Cox proportional hazards model revealed that CRP was significantly associated with PFS and also with OS (hazard ratio (HR) = 1.57, p < 0.001, and HR = 1.63, p < 0.001, respectively). In conclusion, the results of the conducted retrospective study suggest that high baseline level of CRP was independently associated with worse outcome of patients with advanced-stage NSCLC treated with erlotinib. CRP is a commonly used biomarker which is simple and easy to detect, and thus, it is feasible for the use in the routine clinical practice.
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$a Pesek, Milos $u Department of Pneumology, Medical School and Teaching Hospital in Pilsen, Charles University in Prague, Pilsen, Czech Republic.
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$a Finek, Jindrich $u Department of Oncology and Radiotherapy, Medical School and Teaching Hospital in Pilsen, Charles University in Prague, alej Svobody 80, 304 60, Pilsen, Czech Republic.
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$a Topolcan, Ondrej $u Department of Nuclear Medicine, Medical School and Teaching Hospital in Pilsen, Charles University in Prague, Pilsen, Czech Republic.
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$a Racek, Jaroslav $u Institute of Clinical Biochemistry and Hematology, Medical School and Teaching Hospital in Pilsen, Charles University in Prague, Pilsen, Czech Republic.
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$a Minarik, Marek $u Center for Applied Genomics of Solid Tumours, Genomac Research Institute, Prague, Czech Republic. Department of Analytical Chemistry, Faculty of Sciences, Charles University in Prague, Pilsen, Czech Republic.
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$a Benesova, Lucie $u Institute of Clinical Biochemistry and Hematology, Medical School and Teaching Hospital in Pilsen, Charles University in Prague, Pilsen, Czech Republic.
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$a Bortlicek, Zbynek $u Institute of Biostatistics and Analysis, Faculty of Medicine, Masaryk University, Brno, Czech Republic.
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$a Poprach, Alexandr $u Department of Comprehensive Cancer Care, Masaryk Memorial Cancer Institute and Faculty of Medicine, Masaryk University, Brno, Czech Republic.
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