ArticleBiomedical reports2017
The level of serum carcinoembryonic antigen is a surrogate marker for the efficacy of EGFR-TKIs but is not an indication of acquired resistance to EGFR-TKIs in NSCLC patients with EGFR mutationsm.
Article in Biomedical reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Clinical impact of pleural fluid carcinoembryonic antigen on therapeutic strategy and efficacy in lung adenocarcinoma patients with malignant pleural effusion.The Korean journal of internal medicine · 2024Article
- The Prediction Of Epidermal Growth Factor Receptor Mutation And Prognosis Of EGFR Tyrosine Kinase Inhibitor By Serum Ferritin In Advanced NSCLC.Cancer management and research · 2019Article
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Authors and funding
7 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to define the relationship between carcinoembryonic antigen (CEA) and survival in non-small cell lung cancer (NSCLC) patients receiving epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) and to investigate whether the level of serum CEA is related to the mechanism for acquisition of resistance to EGFR-TKIs. A total of 100 patients with advanced NSCLC (stage IIIB or stage IV) and harboring EGFR mutations were included. All patients received erlotinib or gefitinib treatment. The correlation between CEA serum level and clinical benefit from erlotinib or gefitinib treatment was analyzed. Patients were appraised by a review of data from a prospective re-biopsy protocol for lung cancer patients with an EGFR-mutated phenotype with acquired resistance to EGFR-TKI therapy. Of 100 patients, 49 and 21 patients carried high and low level of CEA, respectively; 30 carried normal CEA. Median progression-free survival was 6.4 and 4.5 months in patients with high and low level of CEA, respectively (P=0.027). Median PFS of patients in low-CEA group longer than that of those with normal level of tumors (3.0 months; P=0.002). The difference between groups L and N was not significant regarding objective response rate and overall survival. No significant difference was found in three groups of acquired resistance to EGFR-TKIs. The relative CEA level could predict benefit of EGFR-TKI therapy in advanced NSCLC, but could not predict acquired resistance to EGFR-TKIs.
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