Dr. Hendry received his B.A. (Biology) and M.S. (Physiology) degrees from Northeastern University. His doctoral degree (Biomedical Sciences) was granted from a consortium program that included the Worcester Foundation for Experimental Biology, Clark University, University of Massachusetts Medical School, and Worcester Polytechnic Institute. After postdoctoral training at Vanderbilt University School of Medicine, he joined the faculty and established an independent research program in the Department of Medicine at the University of Arkansas for Medical Sciences. In 1992, he moved his research program to the Department of Biological Sciences at Wichita State University. Since then, he attained the rank of full professor, directed the Department’s graduate program, and received an adjunct appointment as Scientist at the Women’s Research Institute and University of Kansas School of Medicine-Wichita. In 2006, he assumed the role of Departmental chairperson. His scientific focus and expertise is primarily biomedical in nature. For instance, he developed an experimental system that is relevant to two topics of increasing concern in our contemporary society. One of them is well established and focuses on the link between the steroid hormones naturally produced in our bodies and some of the most prevalent forms of human cancer in this country (i.e., estrogen-induced breast, uterine, cervical, and vaginal cancer; plus androgen-induced prostate cancer). The other one has emerged more recently and is most generally known as “endocrine disruption”. It is the result of clinical, laboratory, and field studies that are producing an expanding list of synthetic chemicals and even some natural products that are being classified as putative environmental estrogens or xenoestrogens. At the biomedical, regulatory, and public level, considerable concern surrounds the concept that inappropriate exposure to such agents (especially during the prenatal and/or neonatal period) may disrupt normal reproductive development and function. The possible consequences include an increased incidence of hormone-dependent cancers plus the induction of infertility in both human and wildlife populations. His laboratory is currently examining the potential role of altered epigenetics (DNA methylation, microRNA expression in the phenomena of perinatal endocrine disruption in general and estrogen-dependent cancer in particular. Indeed, this research agenda fits extremely well with the newly recognized paradigm known as the Fetal Basis of Adult Disease or FeBAD.

1) delineate the basic mechanisms whereby estrogen regulates normal patterns of cell proliferation and tissue morphogenesis in reproductive tract organs; and 2) identify causal links between disruption of the normal regulated process and alterations in specific cellular events and molecular factors. We are particularly interested in those alterations that directly initiate or promote carcinogenesis in estrogen target tissues. The experimental system we have used to pursue these objectives was one of several that were originally developed to help understand the cause and perhaps predict the ultimate consequences of a medical catastrophe that emerged in the 1970s. The cause of the catastrophe was that, beginning in the 1950s, the synthetic estrogen diethylstilbestrol (DES) was often administered to pregnant women in the mistaken belief that it would reduce the risk of miscarriage. This practice was abandoned abruptly when, as both the male and female progeny of the DES-treated mothers reached puberty, they began to develop teratogenic and neoplastic lesions throughout their reproductive tracts. Thus, DES can be considered the original perinatal endocrine disruptor or xenoestrogen. We found the hamster to be a convenient and very sensitive model system for studying this phenomenon. Much of our experimental work has focused on the neonatally DES-exposed uterus which, in adulthood, responds to chronic estrogen stimulation with a very high incidence of epithelial-derived tumors (endometrial adenocarcinoma) (1, 2). Our efforts to dissect the mechanism of this phenomenon have revealed important details about neonatal DES-induced uterine disruption, some of which are summarized below: Rapid alterations in the tissue-specific pattern of cell proliferation plus precocious appearance of endometrial glands were observed in the developing (prepubertal) uterus (3). We showed that the hamster cheek pouch is a convenient ectopic site for studies of uterine morphogenesis and endocrine responsiveness (4) and then used it to prove that neonatal DES treatment directly and permanently alters the developing hamster uterus (initiating event) such that it responds abnormally later in life to stimulation (promoting event) with estradiol (E2), the normal ovarian estrogen (5). In the E2-stimulated but preneoplastic adult uterus, the endometrial epithelial compartment was a site of both intense hyperplasia/dysplasia and massive cell death by apoptosis (5). Also in the E2-stimulated but preneoplastic adult uterus, the histopathology observed in the endometrial epithelial compartment was accompanied by alterations in the expression of several genes that are implicated in the control of both cell proliferation (c-jun, c-fos, c-myc) and apoptosis (bax, bcl-2, bcl-x) (6). The uterine disruption profile outlined above was not induced by the same neonatal dose of E2 (7). Our current efforts to probe the mechanism of neonatal DES-induce uterine disruption include: i) the search for genes/proteins that are differentially expressed during both the initiation and promotion phase of the phenomenon, ii) testing the hypothesis that altered patterns of DNA methylation (epigenetic changes) are involved in the phenomenon, and iii) testing the hypothesis that inflammation also contributes to the profile of endometrial dysplasia/neoplasia. Through collaborative arrangements, we have expanded the scope of our investigations in the hamster system. For instance, we have begun to define the effects of neonatal treatment with E2 vs. DES plus other putative endocrine disruptors on the morphogenesis and function of the male reproductive tract (8-10), the cervix (11), and the ovary (12). Two of the important conclusions emerging from our most recent studies are that: 1) The potency of an agent as a perinatal endocrine disruptor depends on characteristics other than its relative estrogenicity, and 2) The disruptive potency and/or mechanism of various putative xenoestrogens differs significantly between the male and female reproductive tract. We are now investigating the potential role of epigenetic mechanisms in the initiation and promotion phases of the reproductive organ disruption phenomena. For instance, we are adapting differential DNA methylation profiling and differential microRNA expression profiling methods to our experimental system.