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Int J Clin Oncol. 2018 Apr;23(2):235-242. doi: 10.1007/s10147-017-1211-1. Epub 2017 Nov 7.

Histological transformation after acquired resistance to epidermal growth factor tyrosine kinase inhibitors.

Author information

1
Department of Medical Oncology, Tianjin Medical University General Hospital, No154 Anshan Road, Heping Dist, Tianjin, 300052, China.
2
Department of Medical Oncology, Tianjin Medical University General Hospital, No154 Anshan Road, Heping Dist, Tianjin, 300052, China. happyonco@163.com.

Abstract

Non-small-cell lung cancer patients with sensitive epidermal growth factor receptor mutations generally respond well to tyrosine kinase inhibitors (TKIs). However, acquired resistance will eventually develop place after 8-16 months. Several mechanisms contribute to the resistance including T790M mutation, c-Met amplification, epithelial mesenchymal transformation and PIK3CA mutation; however, histological transformation is a rare mechanism. The patterns and mechanisms underlying histological transformation need to be explored. We searched PubMed, EMBASE and search engines Google Scholar, Medical Matrix for literature related to histological transformation. Case reports, cases series, and clinical and basic medical research articles were reviewed. Sixty-one articles were included in this review. Cases of transformation to small-cell lung cancer, squamous cell carcinoma, large-cell neuroendocrine carcinoma and sarcoma after TKI resistance have all been reported. As the clinical course differed dramatically between cases, a new treatment scheme needs to be recruited. The mechanisms underlying histological transformation have not been fully elucidated and probably relate to cancer stem cells, driver genetic alterations under selective pressure or the heterogeneity of the tumor. When TKI resistance develops, we recommend that patients undergo a second biopsy to determine the reason, guide the next treatment and predict the prognosis.

KEYWORDS:

Acquired resistance; Epidermal growth factor receptor; Histological transformation; Lung carcinoma; Tyrosine kinase inhibitor

PMID:
29110101
DOI:
10.1007/s10147-017-1211-1
[Indexed for MEDLINE]

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