Over-expression of axl is associated with lung adenocarcinoma and with tumor progression

increased activation of AXL and evidence for epithelial-to-mesenchymal transition in multiple in vitro and in vivo EGFR-mutant lung cancer models with acquired resistance to erlotinib in the absence of the EGFR p.Thr790Met alteration or MET activation

These results indicate that Mer and Axl have complementary and overlapping roles in Non-small cell lung cancer

High expression of receptor tyrosine kinase Axl is associated with lung adenocarcinoma.

Report that miR-374a and miR-548b modulation by Axl regulates tumorigenicity and gefitinib resistance in lung cancer.

Suggest role for Axl signaling in mediating drug resistance and epithelial-to-mesenchymal transition of non-small cell lung carcinoma.

study emphasized that the AXL and EGFR receptor tyrosine kinases were coexpressed in a subgroup of treatment-naive lung adenocarcinomas with or without EGFR mutations

Negative feedback regulation of AXL by miR-34a modulates apoptosis in lung cancer cells by activating the transcription factor ELK1 via the JNK signaling pathway.

High expression level of AXL is associated with lung adenocarcinoma.

Data show that strong AXL expression in surgically resected that lung adenocarcinomas (LADs) was a predictor of poor prognosis.

Study provides evidence that AXL and MET are associated with cell proliferation and metastasis in lung cancer, and the crosstalk between these receptors affects tumor progression.

AXL+ and GAS6+ expression is relevant to a poor prognosis in resected lung adenocarcinoma (AD)patients at stage I. AXL/GAS6 might serve as crucial predictive and prognostic biomarkers and targets to identify individuals at high risk of post-operative death.

these results suggested that Axl, which is regulated by long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1, may exert great influence on invasion and migration of neuroblastoma

we identified YAP-driven AXL overexpression as a mechanism of resistance to EGFR TKIs in lung cancer cells.

AXL was highly expressed in clinical specimens of EGFR-mutated lung cancers and its high expression was associated with a low response rate to EGFR-tyrosine kinase inhibitor. These results indicated pivotal roles for AXL and its inhibition in the intrinsic resistance to osimertinib and the emergence of osimertinib-tolerant cells.

Axl kinase drives immune checkpoint and chemokine signaling pathways in lung adenocarcinomas.

AXL degradation in combination with EGFR inhibition can delay and overcome acquired resistance in human non-small cell lung cancer cells.

AXL Targeting Overcomes Human lung cancer Cell Resistance to NK- and CTL-Mediated Cytotoxicity.

ONO-7475, a Novel AXL Inhibitor, Suppresses the Adaptive Resistance to Initial EGFR-TKI Treatment in EGFR-Mutated Non-Small Cell lung cancer.

The miR6253p/AXL axis induces nonT790M acquired resistance to EGFRTKI via activation of the TGFbeta/Smad pathway and EMT in EGFRmutant nonsmall cell lung cancer.