Table 1.
Tumor Origin | Oncogene(s) | References |
---|---|---|
Bone | • | [125] |
Brain | ••• | [32, 55, 56]a |
Breast | ••• | [22, 33, 72–74, 76–78]b, c, d |
Colon & rectum | • | [40, 126] |
Endometrium | •• | [127] |
Esophagus | • | [128] |
Gastrointestinal tract | • | [86]e |
Kidney | •• | [129, 130]f |
Liver | • | [131] |
Lung | •••• | [23, 66–68]b |
Mantle cell lymphoma | • | [132] |
Ovary | •• | [106, 133] |
Pancreas | • | [24]b |
Pituitary | • | [134] |
Prostate | •• | [28, 37, 123, 135] |
Skeletal muscle | • | [136] |
Skin | •• | [137–139] |
Stomach | ••• | [25, 29, 140]g, h |
Thyroid | •• | [141–143] |
indicates upregulation of Axl; • indicates upregulation of Mer; • indicates upregulation of Gas6; and • indicates upregulation of Protein S.
Coexpression of Axl and Gas6 correlates with poor prognosis.
Overexpression of Axlcorrelates with metastatic cancer and poor prognosis.
Overexpression of Axl is a mechanism of lapatinib resistance in vitro.
Axl expression correlates with ER expression; Gas6 expression correlates with ER and PR activation.
Expression of Axl is associated with imatinib resistance.
Serum Gas6 levels negatively predict survival.
Coexpression of Axl and Mer correlates with poor prognosis.
Overexpression of Gas6 correlates with lymph node metastasis.