Melanoma cells exploit ABL1/2 for drug resistance and immune escape
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Researchers at the University of Kentucky Markey Cancer Center have uncovered a mechanism by which melanoma evades both targeted therapy and the immune system simultaneously. Reporting in Nature Communications, the team shows that melanoma cells use the proteins ABL1 and ABL2 to reactivate ERK signaling, which underlies resistance to MAPK inhibitors, while also secreting chemokines that recruit myeloid-derived suppressor cells (MDSCs) to the tumor. These MDSCs inhibit T cell activity, enabling immune escape. The finding links two previously separate failure modes of melanoma treatment into a single pathway and points to ABL1/2 as a potential target for combination strategies. Follow-up work on therapeutic approaches has not yet been reported.
Written by a model from the reports · updated 2 hours ago
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A University of Kentucky Markey Cancer Center team reports in Nature Communications (DOI: 10.1038/s41467-026-76864-y) that melanoma cells use ABL1/2 to reactivate ERK signaling and secrete chemokines that recruit myeloid-derived suppressor cells (MDSCs) to inhibit T cells, achieving both MAPK inhibitor resistance and immune escape at once.
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