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• W1560400577 abstract "cording to the Common Terminology Criteria for Adverse Events (CTCAE) v4.0, respectively. Afatinib therapy has since continued for 7 months and the patient presently continues to have a good quality of life. We hereby report a patient who successfully underwent a second-line rechallenge with the tyrosine kinase inhibitor (TKI) afatinib. Rechallenge of second-line TKI seems to be a promising option in the treatment of NSCLC patients. Recent reports demonstrate the effectiveness of afatinib against disease progression in patients with common histological types of non-small cell lung cancer who had previously shown clinical benefits from gefitinib and erlotinib [1–3]. However, there have been no reports of successful second-line TKI rechallenge in ADSQ patients after the failure of firstline TKIs. One explanation for the effectiveness of afatinib in in this case could be the ability of afatinib to overcome drug resistance development related to the T790M secondary mutation and the importance of HER2-HER4 [3]. However, we could not perform a rebiopsy to evaluate these secondary mutations, as the patient did not give consent for a bronchoscopy. Tumor heterogeneity in the development of drug resistance might also be a factor. Although the EGFR-mutated cancer cell clones may have been significantly suppressed by the first-generation TKI treatment, they survived treatment with gefitinib and later regrew. At this stage, there are at least 3 clones involved: gefitinib-sensitive EGFR-mutated clones, secondary gefitinib-resistant (e.g. T790M mutation) EGFR-mutated clones, and preexistent resistant clones. Interestingly, recent reports show the effectiveness of reexposure to gefitinib following chemotherapy [4], speculating that the response occurs according to a model of biological selection. When disease progression occurs during chemotherapy treatment following the initial gefitinib treatment, most progressing cancer cells are likely to be EGFR-mutated cancer cells due to the comparatively rapid proliferation rate of this cell population. However, we maintain the belief that afatinib rather than gefitinib rechallenge is the better course of treatment, because afatinib suppresses not only the gefitinib-sensitive EGFR-mutated" @default.
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• W1560400577 date "2015-01-01" @default.
• W1560400577 modified "2023-09-27" @default.
• W1560400577 title "Successful Afatinib Therapy after Resistance to EGFR-TKI in a Patient with Advanced Adenosquamous Cell Lung Cancer" @default.
• W1560400577 cites W2097699101 @default.
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• W1560400577 doi "https://doi.org/10.1159/000431351" @default.
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