Nikki Cheng

The ephrins and Eph receptors in angiogenesis.

Soluble Eph A receptors inhibit tumor angiogenesis and progression in vivo.

Blockade of EphA receptor tyrosine kinase activation inhibits vascular endothelial cell growth factor-induced angiogenesis.

Inhibition of VEGF-dependent multistage carcinogenesis by soluble EphA receptors.

Loss of TGF-beta type II receptor in fibroblasts promotes mammary carcinoma growth and invasion through upregulation of TGF-alpha-, MSP- and HGF-mediated signaling networks.

Genomic and proteomic analysis of mammary tumors arising in transgenic mice.

Inhibition of retinal neovascularization by soluble EphA2 receptor.

Enhanced hepatocyte growth factor signaling by type II transforming growth factor-beta receptor knockout fibroblasts promotes mammary tumorigenesis.

Epidermal growth factor receptor plays a significant role in hepatocyte growth factor mediated biological responses in mammary epithelial cells.

Identification of novel Smad2 and Smad3 associated proteins in response to TGF-beta1.

Transforming growth factor-beta signaling-deficient fibroblasts enhance hepatocyte growth factor signaling in mammary carcinoma cells to promote scattering and invasion.

Abrogation of TGF-beta signaling enhances chemokine production and correlates with prognosis in human breast cancer.

Quantitative analysis of the secretome of TGF-beta signaling-deficient mammary fibroblasts.

Loss of transforming growth factor-beta signaling in mammary fibroblasts enhances CCL2 secretion to promote mammary tumor progression through macrophage-dependent and -independent mechanisms.

Chemokine signaling in cancer: Implications on the tumor microenvironment and therapeutic targeting.

Loss of one Tgfbr2 allele in fibroblasts promotes metastasis in MMTV: polyoma middle T transgenic and transplant mouse models of mammary tumor progression.