Dr. Cheung received her B.Sc. (with 1st class honours) and PhD degrees from the University of Hong Kong. She joined University of Hong Kong as an academic staff after receiving post-doctoral training at the Royal Postgraduate Medical School, London, and the Wolfson Institute of University of Hull on a Croucher Foundation Fellowship. Dr. Cheung’s research interest is cancer biology. Please refer to her selected publications to find out more about her discoveries on the roles and mechanisms of the Id1, Id1-induced IGF2 and microRNAs in promoting esophageal cancer progression.

Dr. Cheung’s research focuses on the molecular mechanisms that promote the development and progression of esophageal squamous cell carcinoma (ESCC). Her team was the first to report that ectopic expression of a helix-loop-helix protein Id1 in cancer cells leads to activation of the phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway, which is involved in regulating a wide spectrum of cellular functions including proliferation, survival, angiogenesis, invasion and metastasis. Their research shows that this mechanism, which also promotes cancer cell stemness and chemoresistance, is mediated by Id1-induced secretion of insulin-like growth factor 2 (IGF2), which exerts autocrine influence on cancer cells via the insulin-like growth factor 1 receptor (IGF1R). They also found that cancer cell-secreted IGF2 can activate stromal fibroblasts in the tumor microenvironment to secrete vascular endothelial growth factor (VEGF), which in turn instigates VEGF receptor 1 (VEGFR1)-positive bone marrow-derived vascular progenitor cells to promote tumor angiogenesis and metastasis. Taken together, these findings substantiate that the Id1/IGF2/VEGF/VEGFR1 cascade plays a pivotal role in tumor-driven pathological processes during cancer progression. These studies also provide important pre-clinical data to support the use of antibodies against IGF2, VEGF2 and their receptors as a novel approach in esophageal cancer therapy. Dr. Cheung’s team also studied the oncogenic role and mechanisms of FBXO31, a member of the F-box protein family, in ESCC. Other recent projects include identification of microRNAs that can reverse chemoresistance and suppress invasion/metastasis of ESCC cells. MicroRNA-377, for example, was found to modulate chemoresistance, and suppress initiation and progression of ESCC by targeting CD133 and VEGF.