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• W3179454984 abstract "Despite current advancements in research and therapeutics, lung cancer remains the leading cause of cancer-related mortality worldwide. This is mainly due to the resistance that patients develop against chemotherapeutic agents over the course of treatment. In the context of non-small cell lung cancers (NSCLC) harboring EGFR-oncogenic mutations, augmented levels of AXL and GAS6 have been found to drive resistance to EGFR tyrosine kinase inhibitors such as Erlotinib and Osimertinib in certain tumors with mesenchymal-like features. By studying the ontogeny of AXL-positive cells, we have identified a novel non-genetic mechanism of drug resistance based on cell-state transition. We demonstrate that AXL-positive cells are already present as a subpopulation of cancer cells in Erlotinib-naïve tumors and tumor-derived cell lines and that the expression of AXL is regulated through a stochastic mechanism centered on the epigenetic regulation of miR-335. The existence of a cell-intrinsic program through which AXL-positive/Erlotinib-resistant cells emerge infers the need of treating tumors harboring EGFR-oncogenic mutations upfront with combinatorial treatments targeting both AXL-negative and AXL-positive cancer cells." @default.
• W3179454984 created "2021-07-19" @default.
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• W3179454984 date "2021-07-13" @default.
• W3179454984 modified "2023-09-29" @default.
• W3179454984 title "An epigenetic switch regulates the ontogeny of AXL-positive/EGFR-TKi-resistant cells by modulating miR-335 expression" @default.
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• W3179454984 doi "https://doi.org/10.7554/elife.66109" @default.
• W3179454984 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8285107" @default.
• W3179454984 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34254585" @default.
• W3179454984 hasPublicationYear "2021" @default.
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