National Cancer Institute
Giovanna Zappalà

Giovanna Zappalà , PhD

Contractor, SAIC-Frederick
Basic Biobehavioral and Psychological Sciences Branch (BBPSB)
Behavioral Research Program (BRP)

Giovanna Zappalà, PhD, was a Medical Affair Scientist in the Basic Biobehavioral and Psychological Sciences Branch (BBPSB), Behavioral Research Program (BRP), Division of Cancer Control and Population Sciences (DCCPS), at the National Cancer Institute (NCI). Dr. Zappalà graduated from the University of Catania College of Pharmacy in Italy, earning a degree in Medicinal Chemistry and Pharmaceutics, and earned a Doctorate in Physiopathology from the University of Rome "Tor Vergata," School of Medicine, in collaboration with the intramural research program at the National Institute of Diabetes and Kidney Diseases (NIDDK).

Dr. Zappalà first joined the intramural ranks of the NCI in 2002 as Postdoctoral Visiting Fellow in the Experimental Transplantation and Immunology Branch (ETIB) where she investigated mechanisms of control of differentiation of adult stem cells into endothelial cells. Later, at NIDDK, she studied molecular mechanisms involved in the pro-apoptotic actions of insulin-like growth factor binding protein-3 in cancer cells. As senior Research Fellow in ETIB she investigated the role of mesenchymal stem cells in thymus regeneration and she worked at the identification of the genes which regulate thymoma onset and progression.

Dr. Zappalà's research interests focused on the elucidation of biological mechanisms through which psychosocial factors, such as stress, depression, and social isolation might influence cancer initiation, progression, invasion, and the metastasis continuum.In particular, she was interested in investigating the influences of the neuroendocrine system on tumor dormancy.

Another area of interest lies at the intersection of early life stress exposure, social isolation, depression, and other psychosocial determinants, and the onset and progression of diseases that involve inflammatory processes such as neurodegeneration and obesity, in a cancer related context. Dr. Zappalà is also interested in the neuroplasticity properties of physical activity and the mechanisms underlying its modulation of stress responsiveness.

Dr. Zappalà was a core member of the NCI Network in Biobehvioral Pathways in Cancer, a transdisciplinary network of scientists aiming to explore the clinical and translational relevance of biopsychosocial determinants and mechanisms of cancer control. Toward the long-term goal of developing independently sustainable research programs, the network facilitates collaborative research among scientists with relevant expertise in cancer biology, basic behavioral science, behavioral medicine, oncology, molecular and cellular biology, stress biologists and methodologists, and other disciplinary perspectives.

Current and past BRP mentors include Paige Green.

Selected Publications and Presentations

Zappalà, G., McDonald, P. G., & Cole, S. W. Tumor dormancy and the neuroendocrine system: An undisclosed connection? . Cancer Metastasis Rev 2012; [ePub Ahead of Print].

Zappalà, G. & Rechler, M. M. IGFBP-3, hypoxia and TNF-alpha inhibit adiponectin transcription. Biochem.Biophys.Res.Commun. 2009; 382(4):785-789.

Zappalà, G., Elbi, C., Edwards, J., Gorenstein, J., Rechler, M. M., & Bhattacharyya, N. Induction of apoptosis in human prostate cancer cells by insulin-like growth factor binding protein-3 does not require binding to retinoid X receptor-alpha. Endocrinology 2008; 149(4):1802-1812.

Shahjee, H., Bhattacharyya, N., Zappalà, G., Wiench, M., Prakash, S., & Rechler, M. M. An N-terminal fragment of insulin-like growth factor binding protein-3 (IGFBP-3) induces apoptosis in human prostate cancer cells in an IGF-independent manner. Growth Horm.IGF.Res. 2008; 18(3):188-197.

Bhattacharyya, N., Pechhold, K., Shahjee, H., Zappalà, G., Elbi, C., Raaka, B., Wiench, M., Hong, J., & Rechler, M. M. Nonsecreted insulin-like growth factor binding protein-3 (IGFBP-3) can induce apoptosis in human prostate cancer cells by IGF-independent mechanisms without being concentrated in the nucleus. J Biol Chem 2006; 281(34):24588-24601.

Last Updated: 04/01/2013 01:25:38