Abstract

Approximately 5% to 10% of EGFR (epidermal growth factor receptor) -mutant non-small cell lung cancers (NSCLCs) develops an acquired resistance to EGFR tyrosine kinase inhibitors with transformation into small-cell lung cancer (SCLC). After the transformation, clinical behavior mimics classic SCLC on many aspects, with frequent but transient responses to platinum-etoposide (EP) or taxanes, modest progression free survival and rare response to immune checkpoint inhibitors. Recently, four SCLC subtypes, defined largely by differential expression of transcription factors ASCL1, NEUROD1, and POU2F3 or low expression of all three transcription factor signatures, were suggested (Gay CM et al, Cancer Cell 2021) (SCLC-A, N, P and I, respectively).

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