Response to erlotinib in a patient with lung adenocarcinoma harbouring the EML4-ALK translocation: A case report
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- Published online on: January 26, 2015 https://doi.org/10.3892/ol.2015.2897
- Pages: 1537-1540
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Copyright: © Alì et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
Lung cancer is the leading cause of cancer‑associated mortality worldwide, and the mainstay of treatment remains to be personalised therapy. Tyrosine kinase inhibitors of the epidermal growth factor receptor (EGFR‑TKIs) have been reported to exert a significant impact in the treatment of non‑small cell lung cancer (NSCLC), particularly in patients harbouring mutations in the EGFR gene. The echinoderm microtubule‑associated protein‑like 4‑anaplastic lymphoma kinase (EML4‑ALK) gene translocation has been described in a subset of patients with NSCLC and possesses potent oncogenic activity. This translocation represents one of the most novel molecular targets in the treatment of NSCLC. Patients who harbour the EML4‑ALK rearrangement possess lung tumours that lack EGFR or K‑ras mutations. The present study reports the case of a patient possessing the EML4‑ALK rearrangement that was initially treated with erlotinib and achieved a lasting clinical response. To the best of our knowledge, the current study is the first report of a clinical response to EGFR‑TKI in a patient with lung adenocarcinoma harbouring the EML4‑ALK fusion gene, but no EGFR mutations. However, as the disease progressed, the ALK gene status of the tumour was investigated, and based upon a positive result, the patient was treated with crizotinib and achieved a complete response. In conclusion, the present study suggests that the EML4‑ALK rearrangement is not always associated with resistance to EGFR‑TKIs. Further studies are required to clarify the biological features of these tumours and to investigate the mechanisms underlying the primary resistance to EGFR‑TKIs when the EML4‑ALK rearrangement is present.
