Chu Chen

For most recent work on differentially expressed genes in oral squamous cell carcinoma, please click the homepage link in the Contact Information section on this page.

A major emphasis of my research has been to understand the possible role of metabolic enzymes in the activation and detoxification of potential carcinogens in the environment, as well as steroid hormones and growth factors, in the etiology of cancer. Of particular interest is the contribution of genetic polymorphisms of these enzymes and receptor molecules for hormones and growth factors to susceptibility to cancer.

In collaboration with epidemiologists, my laboratory has been conducting molecular epidemiologic studies to examine the potential association of polymorphisms of certain genes (such as CYP2D6, CYP2E1, GSTM1, GSTP1, GSTT1, microsomal epoxide hydrolase, NAT1, NAT2, NQO1, etc.), that may play an important role in the activation or detoxification of potential carcinogens that are found in tobacco smoke or are derived from food sources, with the incidence of cancers of the oral cavity, nasopharynx, colon, anus, penis, cervix, vagina, and vulva, and of acute myelocytic leukemia. For cancers of the oral cavity, we are also examining their incidence in relation to alcohol consumption and polymorphisms of the alcohol dehydrogenase type 2 and type 3 genes. Recently, we have begun to use microarray technology to examine differential gene expression in oral cancers of different clinical stage.

Collaborative studies pertaining to hormonal carcinogenesis include: (1) polymorphisms of CYP17, CYP1A1, CYP1B1, catechol O-methyltransferase, glutathione S-transferases, and estrogen receptor in relation to the incidence of cancers of the breast and endometrium; (2) polymorphisms of the 5-alpha reductase type II gene (the 5-alpha reductase converts testosterone to a more potent androgen dihydrotestosterone) and the androgen receptor gene in relation to the incidence of prostate cancer; (3) polymorphisms of CYP11a, CYP17, 3-beta HSD type II, CYP3A4 and UGT2B15 and the incidence of testicular cancer.

Other studies pertain to the evaluation of prediagnostic levels of endogenous sex hormones (androstenedione, testosterone, 3 alpha diol glucuronide, estradiol), sex hormone binding globulin, and insulin-like growth factors and polymorphisms of insulin-like growth factor gene and insulin-like growth factor binding protein gene in relation to prostate cancer risk; the dietary influences on the activities of glutathione S-transferases, cytochrome 450 enzymes, and female hormone levels; the transcriptional regulation of glutathione S-transferases, and the evaluation of melatonin metabolism in relation to exposure to magnetic fields.