Figure 1
Figure 1. Defined oncogenic transformations drive TF expression in cancer. Defined pathways regulating expression of TF in cancer are as follows: (1) Epidermal-to-mesenchymal transformation and TGF-β signaling.11,15 TGF-β indicates transforming growth factor-β; TGFBRI/II, transforming growth factor receptors I and II; and SMAD, contraction of “small” and “mothers against decapentaplegic.” (2) Hypoxia-induced signaling.19 EGR-1 indicates early growth response protein-1. (3) EGFR- and PTEN-dependent pathways.9–11,13 EGF indicates epidermal growth factor; EGFR, epidermal growth factor receptor; and PTEN, phosphatase and tensin homolog. (4) Src-signaling pathways.12 Src indicates Rous sarcoma oncogene cellular homolog12; the c-MET mutation leads to enhanced expression of HGFR (hepatocyte growth factor receptor). (5) Loss of K-ras and p53.7,8,13,14 K-ras indicates V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; P53, protein 53; PI3, phosphatidylinositol-3′; and MAP, mitogen-activated protein.

Defined oncogenic transformations drive TF expression in cancer. Defined pathways regulating expression of TF in cancer are as follows: (1) Epidermal-to-mesenchymal transformation and TGF-β signaling.11,15  TGF-β indicates transforming growth factor-β; TGFBRI/II, transforming growth factor receptors I and II; and SMAD, contraction of “small” and “mothers against decapentaplegic.” (2) Hypoxia-induced signaling.19  EGR-1 indicates early growth response protein-1. (3) EGFR- and PTEN-dependent pathways.9-11,13  EGF indicates epidermal growth factor; EGFR, epidermal growth factor receptor; and PTEN, phosphatase and tensin homolog. (4) Src-signaling pathways.12  Src indicates Rous sarcoma oncogene cellular homolog12 ; the c-MET mutation leads to enhanced expression of HGFR (hepatocyte growth factor receptor). (5) Loss of K-ras and p53.7,8,13,14  K-ras indicates V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; P53, protein 53; PI3, phosphatidylinositol-3′; and MAP, mitogen-activated protein.

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