North Carolina Central University: Nutrition Research Program

NC Central University's Nutrition Research Program is focused on:

  • Use of cancer and diabetes models to study the preventive effects of bioactive food components on cancer and diabetes and its complications;
  • Purification, structure elucidation, bioavailability and biotransformation study of novel bioactive natural products from functional foods and medicinal herbs (such as Traditional Chinese Medicine);
  • Use of chemical and genetic approaches to dissect the molecular mechanism of blood vessel development to suppress cardiovascular diseases and to combat cancers.
  • standardization and quality control of herbal medicine and functional foods;

Dr. TinChung Leung's research focus is to understand the mechanisms by which signaling molecules guide and pattern vascular networks during angiogenesis (formation of new blood vessels), and to exploit the therapeutic potential of chemical modulators (drug-like small molecules and natural products) that will suppress cardiovascular diseases and to combat cancers.


Angiogenesis plays a significant role in human cancer progression and there is a high degree of correlation between microvessel density and Gleason score, pathological stage, and patient survival. Not much is known about the molecular mechanisms underlying tumor induced angiogenesis, the genes or pathways involved in progression or the tumor-stromal interactions which allow tumor progression and establishment of tumor metastases in a new location. Determining the molecular mechanisms underlying tumor induced angiogenesis will enable us to target angiogenic signaling pathways regulating tumor progression.


Zebrafish are used as a vertebrate model system for analyses because of the striking similarity in protein sequences, conserved developmental processes of organogenesis, and the common appearance of pathophysiological processes between zebrafish and human. Phenotypic resemblance of zebrafish gene mutations to human cardiovascular disease as well as physiological responses to drugs exhibited in the zebrafish system provide strong arguments for its use as a model system to study human cardiovascular development and disease. In addition, zebrafish cancer model recapitulates the human disease both molecularly and pathologically.

Dr. Yang's research is on breast cancer etiology and prevention with focuses on the modulation of hormone-growth factor crosstalk, apoptosis and mammary stem cell reprogramming by various genetic and environmental factors. A primary focus is hormonal and dietary modulation of erbB-2 medicated breast carcinogenesis. ErbB-2 (Her2/Neu), a member of the epithelial growth factor receptor (EGFR) family, is overexpressed in about one third of human breast cancers. Using an erbB-2 transgenic mouse model, cell line models and syngeneic tumor transplantation models, we aim to identify novel natural compounds and dietary factors that have chemopreventive and therapeutic effects on erbB-2 overexpressing tumors and mechanisms of various endogenous and exogenous factors that may function as a risk factor in erbB-2 mediated carcinogenesis.

His secondary focus is in utero exposure to bioactive factors on breast cancer risk later in life. Increasing evidence indicates that cancer development could start before birth. Using the MMTV-erbB-2 transgenic mouse model, we explore the molecular mechanisms underlying prenatal exposure mediated carcinogenesis later in life. Our focus is on epigenetic regulation and mammary stem cell reprogramming in premalignant mammary glands.

A third area of research is regulation of apoptosis in breast cancers. Apoptosis, or programmed cell death, has been associated with cancer development and therapeutic resistance. Based on our previous work, we focus on identification and mechanistic understanding of natural compound induced apoptosis to identify novel agents and mechanisms that are synergetic to the existing anti-cancer regimens. We also investigate the mechanisms of apoptosis in cancer cells with mutant p53, particularly the role of p73 and p63 in apoptosis induction and cell cycle arrest, and the coordination between p53-dependent and p53-independent pathways.