AXL

Overview

AXL is a receptor tyrosine kinase of the TAM family (TYRO3, AXL, MERTK) implicated in cancer cell invasion, drug resistance, and immune evasion. In melanoma biology, AXL expression marks an invasive/mesenchymal cell state distinct from the proliferative melanocytic state.

Alterations observed in the corpus

  • AXL expression used as a state marker aligning with the LowMut (neural-crest/invasive) melanocyte subpopulation in a multimodal single-cell atlas of 297 melanocytes from human skin; LowMut melanocytes cluster with the WIMMS “AXL/Neuronal/Invasive” and Belote et al. “MSC” states in cross-study alignment PMID:39975212.
  • Inhibited by cabozantinib alongside MET and VEGFRs in HCC; overexpression associated with tumour progression PMID:24798001
  • Receptor tyrosine kinase associated with epithelial–mesenchymal transition and therapy resistance in NPC; targeted by multi-kinase TKI cabozantinib PMID:24952746
  • Mesenchymal-transition transcript up-regulated in non-responding pretreatment melanoma tumors; co-enriched within the IPRES innate anti-PD-1 resistance transcriptional signature PMID:26997480

Cancer types (linked)

  • MEL — AXL marks the LowMut, neural-crest-like melanocyte subpopulation characterized by clock-like mutational signatures (SBS1/SBS5) and hair-follicle residency; this state has been cross-referenced to the AXL/Neuronal/Invasive transcriptional program in published melanoma atlases PMID:39975212.

Co-occurrence and mutual exclusivity

Therapeutic relevance

  • No direct AXL-targeted therapy is evaluated in the corpus PMID:39975212.

Open questions

  • Whether the AXL/LowMut/neural-crest melanocyte state identified in normal skin represents a precursor to the invasive AXL+ melanoma cell state remains to be tested longitudinally PMID:39975212.

Sources

This page was processed by entity-page-writer on 2026-05-01. - PMID:24798001

This page was processed by wiki-cli on 2026-05-11. - PMID:24952746

This page was processed by wiki-cli on 2026-05-11. - PMID:26997480

This page was processed by entity-page-writer on 2026-05-15.