PT  - JOURNAL ARTICLE
AU  - Zelinski, Daniel P.
AU  - Zantek, Nicole Dodge
AU  - Stewart, Jane C.
AU  - Irizarry, Armando R.
AU  - Kinch, Michael S.
TI  - EphA2 Overexpression Causes Tumorigenesis of Mammary Epithelial Cells
DP  - 2001 Mar 03
TA  - Cancer Research
PG  - 2301--2306
VI  - 61
IP  - 5
4099  - http://cancerres.aacrjournals.org/content/61/5/2301.short
4100  - http://cancerres.aacrjournals.org/content/61/5/2301.full
SO  - Cancer Res2001 Mar 03; 61
AB  - Elevated levels of protein tyrosine phosphorylation contribute to a malignant phenotype, although the tyrosine kinases that are responsible for this signaling remain largely unknown. Here we report increased levels of the EphA2 (ECK) protein tyrosine kinase in clinical specimens and cell models of breast cancer. We also show that EphA2 overexpression is sufficient to confer malignant transformation and tumorigenic potential on nontransformed (MCF-10A) mammary epithelial cells. The transforming capacity of EphA2 is related to the failure of EphA2 to interact with its cell-attached ligands. Interestingly, stimulation of EphA2 reverses the malignant growth and invasiveness of EphA2-transformed cells. Taken together, these results identify EphA2 as a powerful oncoprotein in breast cancer. ©2001 American Association for Cancer Research.