Response to erlotinib in a patient with lung adenocarcinoma harbouring the EML4-ALK translocation: A case report

被引:5
作者
Ali, Greta [1 ]
Chella, Antonio [2 ]
Lupi, Cristiana [1 ]
Proietti, Agnese [3 ]
Niccoli, Cristina [3 ]
Boldrini, Laura [3 ]
Davini, Federico [4 ]
Mussi, Alfredo [5 ]
Fontanini, Gabriella [3 ]
机构
[1] Azienda Osped Univ Pisana, Dept Pathol Anat, I-56126 Pisa, Tuscany, Italy
[2] Azienda Osped Univ Pisana, Dept Pneumol, I-56126 Pisa, Tuscany, Italy
[3] Univ Pisa, Div Anat Pathol, Dept Surg Med Mol Pathol & Crit Care, I-56126 Pisa, Tuscany, Italy
[4] Azienda Osped Univ Pisana, Unit Thorac Surg, I-56126 Pisa, Tuscany, Italy
[5] Univ Pisa, Div Thorac Surg, Dept Surg Med Mol Pathol & Crit Care, I-56126 Pisa, Tuscany, Italy
关键词
EML4-ALK rearrangement; lung adenocarcinoma; erlotinib; crizotinib; SMALL-CELL-LUNG; EGFR MUTATION; FUSION GENE; CANCER; GEFITINIB; KINASE; INHIBITOR; EFFICACY;
D O I
10.3892/ol.2015.2897
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:1537 / 1540
页数:4
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