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. Author manuscript; available in PMC: 2012 May 2.
Published in final edited form as: Expert Opin Ther Targets. 2010 Oct;14(10):1073–1090. doi: 10.1517/14728222.2010.515980

Table 1.

Expression of the receptor tyrosine kinases Axl and Mer and the ligands Gas6 and Protein S in solid tumors.

Tumor Origin Oncogene(s) References
Bone [125]
Brain [32, 55, 56]a
Breast [22, 33, 7274, 7678]b, c, d
Colon & rectum [40, 126]
Endometrium [127]
Esophagus [128]
Gastrointestinal tract [86]e
Kidney [129, 130]f
Liver [131]
Lung [23, 6668]b
Mantle cell lymphoma [132]
Ovary [106, 133]
Pancreas [24]b
Pituitary [134]
Prostate [28, 37, 123, 135]
Skeletal muscle [136]
Skin [137139]
Stomach [25, 29, 140]g, h
Thyroid [141143]

indicates upregulation of Axl; • indicates upregulation of Mer; • indicates upregulation of Gas6; and • indicates upregulation of Protein S.

a

Coexpression of Axl and Gas6 correlates with poor prognosis.

b

Overexpression of Axlcorrelates with metastatic cancer and poor prognosis.

c

Overexpression of Axl is a mechanism of lapatinib resistance in vitro.

d

Axl expression correlates with ER expression; Gas6 expression correlates with ER and PR activation.

e

Expression of Axl is associated with imatinib resistance.

f

Serum Gas6 levels negatively predict survival.

g

Coexpression of Axl and Mer correlates with poor prognosis.

Overexpression of Gas6 correlates with lymph node metastasis.