Allen W Tsang, PhD

Editorial Board Member

Associate Professor
Department of Internal Medicine
Wake Forest School of Medicine,

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My laboratory uses a combination of molecular assays, high-throughput proteomics and imaging technologies to understand the contribution of environmental factors such as infections and diet to cancer pathogenesis and response to therapies. With respect to infectious disease, a particular focus of my research is to investigate the consequence of Chlamydia infection alone or in combination with HPV to cervical, breast and head and neck cancer. My long-term goal is to design and develop interventional and therapeutic strategies to prevent or treat chlamydial infections and chlamydial associated cancer. Investigating Possible Link between Chlamydia and Cancer Chlamydia trachomatis (Ct) and Human papillomaviruses (HPV) are two of the most widespread sexually transmitted diseases (STD) in the world causing an estimated 92 million infections per year with over 2.8 million infections for Ct alone in US. While the large majority of patients respond well to treatment for these infections, a small proportion of these develop cancer later in life. Numerous epidemiological studies conducted over the last decades have shown a positive association between Ct and HPV infections and the presence of premalignant or invasive cancers. Infection with high-risk HPV strains (e.g. HPV16) is now widely acknowledged as important etiological factor in the development of cervical, anal and head and neck squamous cell cancers. Although a number of clinical observations indicate that genital infection with Ct is associated with cervical atypia and cervical neoplasia, the molecular mechanism by which Ct may contribute to the pathogenesis of HPV in cancer is not known. Recently, my laboratory discovered the involvement of EGFR in chlamydial infection. Our studies demonstrate for the first time that chlamydial infection upregulates EGFR expression and activity. This raises the interesting possibility of cooperation between HPV and Ct by which HPV regulates the accumulation of EGF and Ct induces expression of its cognate receptor resulting in hyperactivation of EGFR signaling.

Research Interest

Bacterial Adhesion; Chlamydia trachomatis; Transcriptional Activation; Host-Pathogen Interactions; Receptor, Epidermal Growth Factor