Abstract
The use of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in the treatment of sensitive EGFR mutation in non-small cell lung cancer (NSCLC) has been proved significant curative effect. However, the acquisition of the drug resistance to EGFR-TKIs is almost inevitable, and common drug resistance mechanisms include T790M mutation, cMET amplification, etc. One of the rare resistance mechanisms of EGFR-TKIs is the transformation from NSCLC into small cell lung cancer (SCLC), which account for about 3%-15%. It is an important rare drug resistance mechanism which is not well understood. Therefore, it is necessary to review the present situation and the progress of the this drug resistance mechanism. This article summarizes these hypothesizes from two parts, which are respectively the "common origin" and "transformation time node". At present, two possible mechanisms of this kind of transformation has been proposed, which are respectively the hypothesis of the tumor heterogeneity and the hypothesis of the transformation from NSCLC into SCLC. This article also involves a lot of changes in the level of molecules, such as the lack of RB1 gene, the inactivation of P53 gene and the mutation of PTEN M264I gene, etc. At the same time, this article summarizes the characteristics, the diagnostic methods and the treatment strategy of this kind of transformation. There are still many problems which need further research and resolution.