Fig. 6From: Blockade of PDGFRβ circumvents resistance to MEK-JAK inhibition via intratumoral CD8+ T-cells infiltration in triple-negative breast cancerSchematic model of PDGFRβ switch upon MEK1/2 or JAK2 inhibition in TNBC cells. Under normal physiological condition, PDGFRβ expression is transcriptionally controlled by MYC through MAPK signaling and its protein level is controlled through JAK2 mediated proteolysis (left panel). Upon targeted inhibition of these signaling pathways (i.e. AZD6244, MEK162, BSK805 or AZD1480) results in accumulation of PDGFRβ, driving resistance in breast cancer (right panel), GF: Growth factor; GFR: Growth factor receptorBack to article page